Results 1 to 13 of 13
  1. #1
    Super Moderator sassy69's Avatar
    Join Date
    Feb 2009
    Location
    Plate Junkie
    Posts
    10,633
    Rep Power
    2147943

    Default What is a 17aa steroid?

    You've probably heard of "orals" or 17-alpha alkylated (17aa) steroids. Examples are winstrol, anavar/oxandrolone, dianabol, halotestin, etc. Examples that are NOT 17aa steroids are test propionate, NPP, test enanthate, equipoise, etc.

    These are generally known to be harsh to the liver. Generally speaking, guys are encouraged to NOT run all-oral cycles because of this - primarily because of the dosages men would require. They do use them in conjunction with other injectibles, but keeping the orals to short runs like 4-6 weeks and including liver support (milk thistle, or products like Tyler's Liver Support, LIV 52, etc). Women, on the other hand, very commonly use anavar or winstrol, because they are short esters and will clear quickly, are relatively mild in terms of sides, and do not require injection (i.e. they appear to be just a pill you pop and not a real steroid that requires needles. Less scary. Less "hardcore".) Also at low doses like 10 mg ED, they can be run for longer periods of time, producing nice, maintainable results.

    Here are some references about 17aa steroids:
    Note: as w/ all internet sources, please be intelligent about reading information and keep it context and relative to other things you read.

    http://en.diagnosispro.com/disease_information-for/clinical-manifestations-17-alkylated-steroids-administration-toxicity/10006-104.html

    http://www.usantidoping.org/athletes/cheating_health.html
    "The only way you can hurt the body is not use it. Inactivity is the killer and, remember, it's never too late."
    ~Jack Lalanne



  2. #2
    OLYMPIAN Sistersteel's Avatar
    Join Date
    Feb 2009
    Location
    Strolling down Adrenaline Alley
    Posts
    2,836
    Rep Power
    5760

    Default

    Let me add that Alkylation is what makes oral steroids survive their first pass through the liver as well as what makes them hepatoxic.

    Oral Primo is the only 17 Beta Alkylated oral steroid which makes it relatively less harmful on the liver than the Alpha Alkylated steroids.

  3. #3
    RX MEMBER NPCKnight's Avatar
    Join Date
    Feb 2009
    Posts
    2,559
    Rep Power
    55875

    Default

    Alkalinization?

  4. #4
    Super Moderator sassy69's Avatar
    Join Date
    Feb 2009
    Location
    Plate Junkie
    Posts
    10,633
    Rep Power
    2147943

    Default

    Quote Originally Posted by NPCKnight View Post
    Alkalinization?

    From wikipedia:

    Alkylation is the transfer of an alkyl group from one molecule to another. The alkyl group may be transferred as an alkyl carbocation , a free radical, a carbanion or a carbene (or their equivalents) [1]. Alkylating agents are widely used in chemistry because the alkyl group is probably the most common group encountered in organic molecules. Many biological target molecules or their synthetic precursors comprise of an alkyl chain, with specific functional groups in a specific order. Selective alkylation, or adding parts to the chain with the desired functional groups, is used, especially if there is no commonly available biological precursor.
    "The only way you can hurt the body is not use it. Inactivity is the killer and, remember, it's never too late."
    ~Jack Lalanne



  5. #5
    Super Moderator sassy69's Avatar
    Join Date
    Feb 2009
    Location
    Plate Junkie
    Posts
    10,633
    Rep Power
    2147943

    Default

    http://www.mesomorphosis.com/article...e-steroids.htm



    How to Make Anabolic Steroids Orally-Active?

    by Patrick Arnold Pat is responsible for launching several major product and innovation in the prohormone industry through LPJ Research and Ergopharm, including the first to release androstenedione, 1-AD, 6-OXO, 4-androstenediol, and 19-norandrostenediol. In addition, he is responsible for bringing innovative delivery systems to the prohormone market including HPB cyclodextrin, bioadhesive technology for sustained release, and sustained release sprays.
    The subject of androgenic / anabolic steroids, and the different ways that have been found to make them orally active, has been tossed around lately on the internet mags. This is an interesting topic to the science minded out there, but beyond that, it also has potential utility to the prohormone supplements. The following is my take on the subject, including scientific references and conjecture on my part.
    The problem with natural androgens
    Testosterone is the primary androgen in the human, and is the golden standard by which all other steroids are compared. Unfortunately, testosterone has very poor activity when taken orally. This necessitates that testosterone be administered by extra-oral means such by injection, subcutaneous pellet implant, and transdermal gel or patch.
    17alpha alkylated steroids
    Scientists have developed several synthetic testosterone derivatives that have increased oral bioavailability. The first synthetic alteration that scientists utilized is known as 17 alpha alkylation. 17a alkylation involves the addition of an alkyl group (methyl or ethyl) to the alpha position of the 17 carbon of the steroid backbone. The alkylation at this position prevents the major route of androgen deactivaton – oxidation to a 17-keto steroid - from taking place. This allows a large part of the steroid to avoid liver first pass metabolic degradation. Examples of 17a alkylated steroids are methyltestosterone and Norethandrolone (Nilevar)
    While 17a alkylation is a very effective means of rendering steroids orally active, it suffers from a serious drawback. These steroids are all to some extent toxic to the liver. Some are more toxic than others, but they all have been associated with this problem. Jaundice is not completely uncommon with the usage of this stuff, although this condition is generally confined to individuals who are predisposed to liver problems. Several cases of liver cancer have supposedly been linked to 17a alkylated steroids, however, nothing definitive has been established in this regard. On the other hand, it is somewhat common to observe increases in blood test indicators of liver stress such as BSP retention, and intrahepatic cholestasis (a condition where bile clogs up and stops flowing from the liver).
    While the dangers of 17a alkylated steroids are not trivial, they still comprise some of the most potent anabolic agents available, and therefore their use continues. Most smart bodybuilders are aware of the potential toxicities of these steroids, and therefore they are judicious with their use of them.
    Lipophilic steroid derivatives
    After ingestion, most steroids make their way to the intestines where they are absorbed into the portal circulation. The portal circulation carries the steroid directly to the liver, which is the workhouse of destructive metabolism and inactivation of drugs. As a result, if the steroid is not protected in some way, very little will make it through the liver and into the rest of the body where it can do its magic.
    In addition to the portal route, there is another route through which substances can be absorbed into the body from the intestine. If a substance is lipophilic (fat like) enough it will be absorbed in the same manner that dietary fat is. Dietary fat is incorportated into chylomicra, which are small fat globules composed of protein and fat. These chylomicra are absorbed into the lymphatic circulation, which by passes the liver. If you make a steroid lipophilic enough by altering its structure, then it too will incorportate into chylomicra and absorb into the lymphatic system. Once in the lymphatic system it can cross over into the general blood circulation, making it there without being subjected to the massive metabolic breakdown in the liver.
    Scientists have found that by adding lipophilic side chains to steroids, they will to some extent be absorbed into the lymphatic system. If the side chain is linked on in such a way that it can hydrolyze (break apart) easily after being absorbed, the steroid is essentially rendered orally active. Two side chains that have been utilized to increase the oral bioavailability of steroids through increased lymphatic absorption are long chain alkyl ester groups, such as is seen with testosterone undecanoate (andriol), and enyl ether groups, such as is seen with quinbolone (anabolicum vaster).
    "The only way you can hurt the body is not use it. Inactivity is the killer and, remember, it's never too late."
    ~Jack Lalanne



  6. #6
    Super Moderator sassy69's Avatar
    Join Date
    Feb 2009
    Location
    Plate Junkie
    Posts
    10,633
    Rep Power
    2147943

    Default

    The term "orally active" is of course a relative term. Lipophilically modified steroids are more orally active than the free parent steroids, however, they are no where near as active as the 17alpha-alkylated steroids. Testosterone undecanoate (TU) is probably the most commonly known lipophilically modified androgen, and it is not considered a very potent compound (its recommended daily dosage is about 240mg). In fact, one study found the oral administration of testosterone undecanoate led only to an absolute testosterone bioavailability of 6.83 +/- 3.32%. That is very slight, especially considering the fact that in the same study they found the bioavailability of straight testosterone to be 3.56 +/- 2.45% (Eur J Drug Metab Pharmacokinet 1986 Apr-Jun;11(2):145-9). That means TU is just a little less than twice as orally active as free testosterone, which is unimpressive to say the least.
    The other problem with lipophilic steroid preparations is the high variability in absorption from one person to another. In other words, one guy might absorb the stuff very well while the other guy might absorb very little. There is also high variation within individuals themselves, depending on their gastrointestinal condition when they take the stuff. In another study, ten post-menopausal women were given 40 mg of TU and their peak blood values were recorded. The values varied widely - more than ten fold (range: 5.8-64.0 nmol/L) - amongst the subjects (J Clin Endocrinol Metab 1998 Nov;83(11): 3920-4).
    There is no specific data I can find on the bioavailabilty of enyl ether compounds, but since their mode of action is identical to long chain alkyl ester compounds like TU, it is a fair assumption that they too are not outstandingly high in oral bioavailability, or in consistency of absorption. What I do know is that the one and only enyl ether oral steroid on the market today (quinbolone) is generally regarded by european bodybuilders / athletes as too weak to even bother taking.
    Ring A modified steroids
    There is one more class of anabolic / androgenic steroids that are orally active. These have unique structural modifications in the steroid A ring. What these modifications do is help preserve the steroids 17beta hydroxyl group, and minimize oxidation to the inactive 17-keto form.
    Androgens such as testosterone exist in the body in an equilibrium between their active 17beta hydroxyl form and the inactive 17-keto form.
    Normally, the equilibrium lies pretty far to the right (formation of inactive 17 keto steroid), however some steroids have certain modifications made in the A ring that alter this equilibrium by shifting it heavily to the left (towards the formation of active 17beta hydroxyl steroid).
    The most common A-ring modifications that shift the 17beta hydroxyl / 17-keto equilibrium to the left are methylation at the 1alpha position, and unsaturation (double bond) in the 1(2) position (Acta Endocr, 41, (1962) 494). Examples of orally active steroids that contain one or more these modifications include methenolone (Primobolan), mesterolone (Proviron), and 1-testosterone.
    You probably have heard of mesterolone and methenolone, but it is doubtful you have ever heard of 1-testosterone. 1-testosterone is a very interesting compound, not just because it is orally active but also because it is very anabolic. It has been reported to be over 7 times as anabolic as testosterone in a study funded by the pharmaceutical giant Searle (J Org Chem, 27 (1962) 248). Furthermore, being a 5alpha reduced steroid, it should not aromatize to estrogens.
    "The only way you can hurt the body is not use it. Inactivity is the killer and, remember, it's never too late."
    ~Jack Lalanne



  7. #7
    Super Moderator sassy69's Avatar
    Join Date
    Feb 2009
    Location
    Plate Junkie
    Posts
    10,633
    Rep Power
    2147943

    Default

    Clipped from http://www.ironmagazine.com/anabolic_steroids.php


    Types of Steroids

    Below we've compiled a list of some anabolic steroids, including their relative potency and some other info. Sometimes, the names of steroids can be confusing to a newbie. This is because you have the chemical name, the various brand names, and the slang or street names for each product.

    For example, methandrostenolone is known to most people as Dianabol, but you probably hear it referred to as D-bol. Of course, you'll likely be using the veterinary version called Reforvit-B, whose street name is Reffie or Reffie-B. Got all that? Don't worry, the more you read the more you get used to all the terminology. To help you out, I've listed the chemical name as well as a few of the trade names for each 'roid.

    Fluoxymesterone (Halotestin, Stenox)

    This is a 17-alpha alkylated steroid. In other words, it's been altered in order to withstand the liver's "first pass" metabolism to a better degree, i.e., the liver doesn't inactivate the stuff before it can exert its effects. Without this alkylation, you'd need much higher concentrations to get results, as is the case with any 17-AA. Anyhow, this steroid appears to have a lower affinity for the AR, but can agonize the receptor at higher dosages.

    As far as "real world" effects, fluoxymesterone has a reputation for increasing strength to a large degree. However, gains in muscle mass on this steroid aren't very great. In clinical settings, dosages range from 2.5 mg to 40 mg a day in divided dosages. However, bodybuilders have been known to use from 30 to 80 mg per day. It has a half-life of approximately 9.2 to 10 hours. (I'll talk about why knowing about half-lives is important later.) Oh yeah, and it doesn't aromatize. This means it's not likely to convert to estrogen, the female hormone. In the real world, that means the risk getting gyno (bitch tits, i.e. breast tissue growth in males) is small to nonexistent.

    Methandrostenolone (Dianabol, Reforvit, Anabol)

    This 17-AA steroid was the first to be introduced to athletes in the 50s. Bodybuilders caught on soon after, no doubt. It's aromatizable, and therefore can increase estrogen levels. Since it doesn't bind very well to the AR, it's thought that it works by antagonizing the effects of catabolic glucocorticoids.

    D-bol has a great reputation for increasing both size and strength to a pretty good degree. While the half life isn't readily available in the literature, it can be assumed through deductive reasoning that it's around four to seven hours. Bodybuilders typically use around 25 to 100 mg per day depending on whether it's used alone or in conjunction with another steroid (a practice called stacking).

    Stanozolol (Winstrol)

    This steroid is also17-AA. It can't aromatize and doesn't bind very well to the AR. Consequently, it's likely to exert its anabolic effects in a similar fashion to that of methandrostenolone. In other words, it affects glucocorticoids in a beneficial manner.

    Another benefit may be its ability to antagonize or block progesterone from binding to receptors. Progesterone is one of the reasons why certain anabolics cause water retention.

    Stanozolol has a great reputation for increases in strength as well as moderate increases in muscle mass. Actually, these "moderate" gains are rather impressive, considering that this drug doesn't cause much water retention. In clinical settings, typical dosages are between 2 to 6 mg daily. In order to see desired effects, bodybuilders typically consume between 25 to 100 mg daily. While I can't locate any literature on its half-life, based on its molecular composition it would seem to have a slightly longer half-life than most of the other orals. I'd say it's likely to be in the range of 7 to15 hours.

    Oxandrolone (sold as oxandrolone powder or Oxandrolona)

    This is yet another 17-AA. It won't aromatize but appears as though it will bind to the AR as long as the dosages are high enough. It has a reputation for increasing strength gains, as well as having a "hardening" effect. This is supported somewhat, as oxandrolone was shown to reduce subcutaneous fat to a greater degree than Testosterone. Whether this is an inherent property of all 17-AA steroids or an effect that's unique to oxandrolone, I'm not sure.

    Oxandrolone, along with most of the other synthetic steroids, are thought to be equally (if not more) anabolic than Testosterone on a milligram per milligram basis, while minimizing androgenic side effects. Oxandrolone was shown to have approximately six times the anabolic effect of methyltestosterone in human subjects, following oral doses. Oxandrolone may also increase the number of skeletal muscle androgen receptors.

    In clinical settings, dosages have ranged from 1.25 to 80 mg per day. Bodybuilders may take anywhere from 25 to 160 mg per day. The half-life is approximately nine hours.

    Methenolone Acetate and Enanthate (Primobolan)

    This steroid doesn't aromatize and can either be ingested via the acetate version or injected via the enanthate. This steroid does bind rather well to the AR and is known for its mild gains in muscle mass. Still, considering that it'll cause next to zero water retention, these gains are rather good. (Note that some bodybuilders think certain steroids work better based solely on the weight they gain. In actuality, they could be just retaining a lot of water along with the muscle gains. These are the same guys who think they "lose" a lot of muscle after their cycle is completed, when they actually just lost much of the water they'd been holding.)

    Clinical dosages that are commonly seen with methenolone range from 10 to 20 mg daily, sometimes a little higher for the oral version. For the enanthate version, dosages are usually 100 mg every two to four weeks. Bodybuilders typically use 400 to 1000 mg a week. The half-life appears to be very similar to Deca, perhaps slightly shorter. So with this in mind, I'd say the half-life would be around five to seven days.

    Oxymetholone (Anadrol)

    This 17-AA steroid can't aromatize, but has been known to have progestenic properties and thus, can cause water retention. It has a great reputation for increasing muscle mass and strength to a large degree. It's also thought to have a very high anabolic/androgenic ratio.

    The typical dosage in clinical settings is one to five milligrams per kilogram of bodyweight per day. So, a 150 pound person would consume anywhere from 68 to 341 mg per day. However, the higher dosages aren't employed that often. Bodybuilders typically consume around 50 to 150 mg per day. While I can't find info on the half-life in the formal literature, it would seem it's similar to that of stanozolol. Obviously, this isn't a hard fact, but the half-life should be right in the neighborhood of 7 to15 hours. Only God and Bill Roberts know for sure.

    Testosterone Enanthate, Cypionate, Propionate, Suspension (commonly called "T")

    This steroid can aromatize and binds well to the AR. It's well known for its ability to produce great gains in muscle size and strength, provided that the dosages are high enough. It does cause quite a bit of water retention and has quite a few side effects when compared to the other anabolics.

    Clinical dosages vary, but cypionate and enanthate are both injected every two to three weeks at dosages of around 200 to 300 mg. Propionate and suspension aren't preferred as they don't provide that long of a sustained release. Bodybuilders typically use around 500 to 1,000 mg per week. The cypionate ester has a half-life of around eight days. Enanthate is just slightly shorter and propionate is quite a bit shorter. By the way, Testosterone in a suspension has a half-life of only 10 to 100 minutes.

    Nandrolone Decanoate and Laurate (usually referred to as Deca)

    This steroid binds very well to the AR and doesn't aromatize. It can produce moderate gains in muscle mass with little water retention. However, it, like oxymetholone, can be progestenic leading to water retention when higher dosages are used.

    In clinical settings, dosages are around 50 to 100 mg every three to four weeks. Bodybuilders use around 300 to 800 mg per week. The decanoate ester has a half-life of six to eight days and the laurate ester commonly seen in veterinary products has a slightly longer half-life.
    "The only way you can hurt the body is not use it. Inactivity is the killer and, remember, it's never too late."
    ~Jack Lalanne



  8. #8
    Super Moderator sassy69's Avatar
    Join Date
    Feb 2009
    Location
    Plate Junkie
    Posts
    10,633
    Rep Power
    2147943

    Default

    http://www.bodybuilding.com/fun/par19.htm

    By: Roy Harper

    NOTE: The opinions below are the author's only and may not represent the opinion of Bodybuilding.com. It is important for you to research all sides of an issue and consult your doctor before taking any medical advice.
    We all know that the alpha alkylated steroids are hepatotoxic, right... But, is there actually any truth to this? We've been told for years that if you take 17 alpha-alkylated steroids, you will eventually run into liver problems. Never combine 17 aa's, never go beyond 50mg day, never go longer than 4 weeks, etc. All of this is crap! As I we walk you through some studies, today, you'll see 17 alpha-alkylated steroids can be hepatotoxic but not to the degree you would think.

    To make a steroid hepatotoxic, you need only a small change to a steroid molecule; A strong bond that cannot readily be down broken by enzymes in the liver. This may be a bond at the 17th position, or even at the 1st position (as in methenolone or proviron). Because the liver cannot easily break the steroid down before it is released in to the blood stream, this also results in the steroid to becoming more orally bio-available.
    We can see that the liver has to work harder to break down these steroids. Enzymes in the blood and tissue easily metabolize other steroids such as Testosterone. Commonly, this increase in liver activity has been viewed as a harmful process, but as you will see, this increase is, in and of itself, irrelevant. The liver is THE filter of the human body -- it can figure out what to do with just about anything. The only real problem comes in when one keeps their liver at full blast for long periods of time.
    Let's look at some studies showing the hepatotoxicity of steroids. Here's one of my favorites, a study published in 1979[1]. Essentially, researches did a study of deaths caused by hepatic angiosarcoma (a malignant tumor of vascular tissue in the liver) between 1964 and 1974. Researchers found 131 reported cases of death from hepatic angiosarcoma. Out of the 131 cases, 3.1% (4 cases) were reported to be at all related to the use of androgenic-anabolic steroids. Keep in mind that these 4 people could have liver complications before any steroids were used, aka a genetic disposition. In fact there is no proof, in this study at least, that the anabolic-androgenic steroids even caused the hepatic angiosarcoma.
    This is the classic case of associating a cause with an effect, without any evidence, aside from both existing. Furthermore, based on the above numbers, there are only 0.4 cases of hepatic angiosarcoma reported each year, by those using AAS. Now consider the number of people on steroids at this time. Now factor in all the people that don't know their ass from a hole in the ground when it comes to using AAS, properly. Clearly, this is very week evidence. Lastly there has not been a real increase in hepatic angiosarcoma since the early seventies. Meanwhile, there has been a huge, almost exponential, increase in steroid use during this period.
    Another study, that somewhat supports the previous hepatotoxicity case, showed the possibilities of hepatic adenomas(cysts in the liver) caused by androgenic-anabolic steroids[2]. In this study, a Japanese girl was found to have multiple liver lesions after the use of the drug oxymetholone (aka Anadrol).
    Most everyone "knows" that Anadrol is linked with liver problems, but a closer inspection into this study shows more. Apparently, this girl, starting at the age of 14, was diagnosed with aplastic anemia. She was prescribed oxymetholone at 30mg per day. This continued for 6 years until the lesions first appeared. Assuming that the girl was most likely around 100 lbs., this was a pretty heavy dosage. If you extrapolated this data out to a 200 - 250lbs. male, that would be taking approximately 60 - 90mg of anadrol per day for 6 years. Ouch!
    The researchers also stated that there were only 17 other cases of hepatic adenomas, found in English literature between 1975 and 1998. They failed to mention the causes of these 17 cases, but there is no reason to believe they were all using 17-AA androgens and 17 is certainly miniscule compared to the number of people who have used them. The authors' finish off the study by saying the following: "This report may be helpful in identifying the population who is at risk of developing hepatic sex hormone-related tumors." So remember, if you're a small 14-year-old girl taking 30mg of Anadrol per day for 6 years, you may be at risk!
    Let's move on to some more useful studies. Take for example a 1995 study that showed the toxic effects of anabolic-androgenic steroids in primary rat hepatic cell cultures[3]. In this study the researchers used the following drugs and dosages:
    The Study
    Steroid
    1x10^-8M
    1x10^-6M
    1x10^-4M
    19-nortestosterone
    0.002744mg
    0.2744mg
    27.44mg
    Fluoxymesterone
    0.003365mg
    0.3365mg
    33.65mg
    Testosterone cypionate
    0.004126mg
    0.4126mg
    41.26mg
    Stanozolol
    0.003285mg
    0.3285mg
    32.85mg
    Danazol
    N/A
    N/A
    N/A
    Oxymetholone
    0.003325mg
    0.3325mg
    33.25mg
    Testosterone
    0.002884mg
    0.2884mg
    28.84mg
    Estradiol
    0.0027424mg
    0.2724mg
    27.24mg
    Methyltestosterone
    0.003024mg
    0.3024mg
    30.24mg

    As proof of the hepatoxicity they used Lactate dehydrogenase release, neutral red retention, and glutathione depletion to determine plasma membrane damage, cell viability, and possible oxidative injury, respectively.
    What they showed was that the 17 alpha-alkylated steroids, methyltestosterone, stanozolol and oxymetholone, significantly increased Lactate dehydrogenase release and decreased neutral red retention at the 1x10^-4M dosage for 24h. Both methyltestosterone and oxymetholone also showed depleted glutathione at the 1x10^-4M dosage after 2h, 6h and 8h treatments. In other words they increased liver activity. You may also note that the other, non-alkylated steroids showed no significant difference in any levels. All in all this not only shows that 17 alpha-alkylated steroids are directly "hepatotoxic", but also non-alkylated steroids are note hepatotoxic at all. But is this a real measure of hepatotoxicity? There is yet to be any correlation between the increase of the above-mentioned measurement and "hepatotoxicity". Obviously, high dosages of the 17 alpha-alkylated steroids are potentially dangerous, but upon closer inspection, the study reveals more.
    Take a look, the researchers took cell cultures from the liversse of 60-day-old Sprague-Dawley rats. Not only are rat livers much smaller than human livers, but these were merely cultures. Furthermore, it was the 1x10^-4M concentrations that caused the most changes, but these are approximately 1 to a 1/3 of a full, daily human dosage -- at least for the 17 alpha-alkylated steroids. Even at the 1x10^-6M concentration, there were no significant changes observed. It's apparent that the levels of 17 alpha-alkylated steroids used were potentially toxic, but for a human to take the same amount would be insane. I'm guessing this could translate to maybe 4 grams every 24 hours or 28 grams a week if not more.
    What is common so far is we can only prove that any steroid, that is believed to be hepatotoxic, only increases liver activity. I'll say it again, where is the correlation to hepatotoxicity? We know that if the liver is running at 100% for long periods this may cause complications, but this is akin to any other chemical, which is metabolized by the liver. Ever noticed that liver cancer due to alcoholism takes decades of constant alcohol abuse? It's apparent that the possibility for hepatotoxicity is there, but for the smart steroid user this is nearly an impossible task.
    Another study done in 1999, attempted to show the acute and chronic effects of stanozolol on the liver[4]. In acute treatments of stanozolol, dosages not mentioned, both cytochrome P456 and b5 (microsomal enzymes) levels dropped after 48 hours, and then at 72 hours, levels significant increased. On the other hand, with chronic treatments, time or dosage not mentioned, these microsomal enzymes showed a decrease in levels. Researchers showed that both acute and chronic treatments resulted in "slight to moderate inflammatory or degenerative lesions in centrilobular hepatocytes", but the authors did not note true hepatotoxicity.
    How about we look at the other side of the story, the good studies. For instance, in a 1999 study, which looked at the effects of an 8-week cycle of 17 alpha-alkylated steroids[5]. The researchers used fluoxymesterone, methylandrostanolone, or stanozolol on rats at 2mg/kg-body weight, five times a week for 8 weeks. That's 182mg per dosage, for a 200lb man, or 910mg per week. Half of the rats were sedentary and the other were trained on a treadmill.
    Levels of NADH-cytochrome c reductase, succinate cytochrome c reductase, and cytochrome oxidase (showing liver activity), increased in the steroid-administered rats, while citrate synthase showed no change. Comparatively, in vitro, the "cytochrome oxidase and citrate synthase activities were insensitive to the AAS, whereas NADH-cytochrome c reductase and succinate cytochrome c reductase activities were partly inhibited."
    Furthermore, in vivo, each rat had liver enzyme levels that were within normal range. From this, the researchers determined that the steroid-administered rats, trained or sedentary, did not show "...classical serum indicators of hepatic function". Extrapolating this, 910mg a week for 8 weeks could potentially have little to no effect on the liver in humans.
    As for human studies, in 1999 researchers tried to prove that the hepatotoxicity of steroids is overstated[6]. In this study, 15 of the participants were bodybuilders using self-administered steroid dosages and 10 were non-steroid bodybuilders. Serum data was compared to 49 patients with viral hepatitis, and 592 exercising and non-exercising medical students.
    All of the bodybuilders showed increases in aspartate aminotransferase (AST), alanine aminotransferase (ALT) and creatine kinase (CK) while gamma-glutamyltranspeptidase (GGT) levels were in the normal range. In comparison, hepatitis patients showed increased ALT, AST, and GGT levels while the control exercising medical students showed increased CK levels. From this, the researchers suggested that it is the correlation between AST, ALT and GGT that shows true liver dysfunction. Keep in mind, we can only guess that the 15 steroid users were using 17 alpha-alkylated steroids, and we do not know what the dosages that were used., but common sense tells us the results are likely relevant.
    Last but not least, a simple study done in 1996, showed the long term benefits after taking a 3 month break from steroids[7]. 16 bodybuilders using steroids were compared to 12 bodybuilders that were not. After a three-month drug withdrawal, the researchers showed that levels of liver enzymes, types not mentioned, returned to the same as the non users. Again the dosages are left to the reader's imagination and we can only guess that the 16 steroid users were using 17 alpha-alkylated steroids.
    So What Can We Conclude From All Of This?
    First off, 17 alpha-alkylated steroids are hepatotoxic in high dosages taken for a long time. On the other hand, short cycles and small dosages appear to be perfectly safe. I suggest that maximum dosages should be 500mg to 900mg per day. They should be cycled for perhaps 8 weeks at a time, and if needed a 3-month break from them should be used. Using the above-mentioned techniques, your liver can be healthy for a long time. Simply put, the hysteria surrounding "hepatoxic" steroids, is based mainly on folk lore.
    This article appears courtesy of www.mindandmuscle.net
    References: [1] Lancet 1979 Nov 24;2(8152):1120-3, Hepatic angiosarcoma associated with androgenic-anabolic steroids. Falk H, Thomas LB, Popper H, Ishak KG.
    [2] J Gastroenterol 2000;35(7):557-62, Multiple hepatic adenomas caused by long-term administration of androgenic steroids for aplastic anemia in association with familial adenomatous polyposis. Nakao A, Sakagami K, Nakata Y, Komazawa K, Amimoto T, Nakashima K, Isozaki H, Takakura N, Tanaka N.
    [3] J Pharmacol Toxicol Methods 1995 Aug;33(4):187-95, Toxic effects of anabolic-androgenic steroids in primary rat hepatic cell cultures. Welder AA, Robertson JW, Melchert RB.
    [4] Arch Toxicol 1999 Nov;73(8-9):465-72, Evaluation of acute and chronic hepatotoxic effects exerted by anabolic-androgenic steroid stanozolol in adult male rats. Boada LD, Zumbado M, Torres S, Lopez A, Diaz-Chico BN, Cabrera JJ, Luzardo OP.
    [5] Med Sci Sports Exerc. 1999 Feb;31(2):243-50, Rat liver lysosomal and mitochondrial activities are modified by anabolic-androgenic steroids. Molano F, Saborido A, Delgado J, Moran M, Megias A.
    [6] Clin J Sport Med 1999 Jan;9(1):34-9, Anabolic steroid-induced hepatotoxicity: is it overstated? Dickerman RD, Pertusi RM, Zachariah NY, Dufour DR, McConathy WJ.
    [7] Int J Sports Med 1996 Aug;17(6):429-33, Body composition, cardiovascular risk factors and liver function in long-term androgenic-anabolic steroids using bodybuilders three months after drug withdrawal. Hartgens F, Kuipers H, Wijnen JA, Keizer HA.
    "The only way you can hurt the body is not use it. Inactivity is the killer and, remember, it's never too late."
    ~Jack Lalanne



  9. #9
    Super Moderator sassy69's Avatar
    Join Date
    Feb 2009
    Location
    Plate Junkie
    Posts
    10,633
    Rep Power
    2147943

    Default

    http://www.bodybuildingweb.net/blog/...e-on-steroids/


    Liver Protection while on Steroids

    July 7th, 2007 by Paul Johnson


    All anabolic steroids put stress on the liver. So does alcohol, prescription drugs, and asprin. This is the reasoning behind bodybuilding veterans not recommending “oral only cycles”. Oral steroids are methylated in order to bypass breakdown by the liver. As a result they are highly toxic to the liver.
    The reason why injectable steroids are recommended by mainstream bodybuilders to be the base of a steroid cycle is because it is much easier on the liver. Injectable steroids are not methylated and they slowly release over days putting much less stress on the liver.
    If you want an equivalent anabolic effect of a oral steroid as you get with injectables you will be putting your liver under a lot more stress. The liver is a very resilient organ and can even grow back if it’s severed or damaged. However, there is no reason to put your liver under undue stress by using mainly orals.
    Recommended liver supplements on cycle
    Milk thistle is a general liver health supplement. NAC seems to be even more important in helping against liver detoxification and healing. Keep in mind that liver supplements (in theory) should reduce the potency of your steroids. Many bodybuilders for this reason do not take them during their cycle. I think it’s a good idea to use low doses of NAC and milk thistle even while on cycle. Frequent steroid users should use liver health supplements everyday year around. Here is a list of all the liver health supplements currently on the market.
    "The only way you can hurt the body is not use it. Inactivity is the killer and, remember, it's never too late."
    ~Jack Lalanne



  10. #10
    Super Moderator sassy69's Avatar
    Join Date
    Feb 2009
    Location
    Plate Junkie
    Posts
    10,633
    Rep Power
    2147943

    Default

    http://www.ingentaconnect.com/conten...00014/art00003

    Drugs 2001;61(14):2035-63 Related Articles, Links


    The use of silymarin in the treatment of liver diseases.

    Saller R, Meier R, Brignoli R.

    Abteilung Naturheilkunde, University Hospital Zurich, Switzerland.

    The high prevalence of liver diseases such as chronic hepatitis and cirrhosis underscores the need for efficient and cost-effective treatments. The potential benefit of silymarin (extracted from the seeds of Silybum marianum or milk thistle) in the treatment of liver diseases remains a controversial issue. Therefore, the objective of this review is to assess the clinical efficacy and safety of silymarin by application of systematic approach. 525 references were found in the databases, of which 84 papers were retained for closer examination and 36 were deemed suitable for detailed analysis. Silymarin has metabolic and cell-regulating effects at concentrations found in clinical conditions, namely carrier-mediated regulation of cell membrane permeability, inhibition of the 5-lipoxygenase pathway, scavenging of reactive oxygen species (ROS) of the R-OH type and action on DNA-expression, for example, via suppression of nuclear factor (NF)-kappaB. Pooled data from case record studies involving 452 patients with Amanita phalloides poisoning show a highly significant difference in mortality in favour of silibinin [the main isomer contained in silymarin] (mortality 9.8% vs 18.3% with standard treatment; p < 0.01). The available trials in patients with toxic (e.g. solvents) or iatrogenic (e.g. antispychotic or tacrine) liver diseases, which are mostly outdated and underpowered, do not enable any valid conclusions to be drawn on the value of silymarin. The exception is an improved clinical tolerance of tacrine. In spite of some positive results in patients with acute viral hepatitis, no formally valid conclusion can be drawn regarding the value of silymarin in the treatment of these infections. Although there were no clinical end-points in the four trials considered in patients with alcoholic liver disease, histological findings were reported as improved in two out of two trials, improvement of prothrombin time was significant (two trials pooled) and liver transaminase levels were consistently lower in the silymarin-treated groups. Therefore, silymarin may be of use as an adjuvant in the therapy of alcoholic liver disease. Analysis was performed on five trials with a total of 602 patients with liver cirrhosis. The evidence shows that, compared with placebo, silymarin produces a nonsignificant reduction of total mortality by -4.2% [odds ratio (OR) 0.75 (0.5 - 1.1)]; but that, on the other hand, the use of silymarin leads to a significant reduction in liver-related mortality of-7% [OR: 0.54 (0.3 - 0.9); p < 0.01]. An individual trial reported a reduction in the number of patients with encephalopathy of -8.7% (p = 0.06). In one study of patients with cirrhosis-related diabetes mellitus, the insulin requirement was reduced by -25% (p < 0.01). We conclude that available evidence suggests that silymarin may play a role in the therapy of (alcoholic) liver cirrhosis. Silymarin is has a good safety record and only rare case reports of gastrointestinal disturbances and allergic skin rashes have been published. This review does not aim to replace future prospective trials aiming to provide the 'final' evidence of the efficacy of silymarin.



    -----------------------------------------------------



    http://www.ncbi.nlm.nih.gov/pubmed/12427501
    Am J Med 2002 Oct 15;113(6):506-15 Related Articles, Links


    Milk thistle for the treatment of liver disease: a systematic review and meta-analysis.

    Jacobs BP, Dennehy C, Ramirez G, Sapp J, Lawrence VA.

    Department of Medicine, University of California, San Francisco 94143, USA. [email protected]

    PURPOSE: Milk thistle, an herbal compound, is the dietary supplement taken most frequently by patients with chronic liver disease. We performed a systematic review of the literature to determine the efficacy and safety of this herb for the treatment of liver disease. METHODS: We searched English and non-English reports through July 1999 using thirteen databases and reference lists, and contacting manufacturers and technical experts. Reviewers independently screened all reports to identify randomized placebo-controlled trials that evaluated milk thistle for the treatment of liver disease. Outcomes of primary interest included mortality, histological findings on liver biopsy specimens, serum aminotransferase and albumin levels, and prothrombin times. RESULTS: Fourteen trials met inclusion criteria. Four trials reported outcomes for mortality among 433 participants. The overall summary odds ratio for mortality in the milk thistle group compared with placebo was 0.8 (95% confidence interval [CI]: 0.5 to 1.5; P = 0.6). Three trials assessed histology on liver biopsy; study quality was inversely associated with the likelihood of histological benefit for milk thistle compared with placebo. There were no differences in serum alanine aminotransferase, aspartate aminotransferase, or albumin levels, or prothrombin times, among participants assigned to milk thistle compared with those assigned to placebo. The only statistically significant difference was a greater reduction in alanine aminotransferase levels among patients with chronic liver disease assigned to milk thistle (-9 IU/L, 95% CI: -18 to -1 IU/L; P = 0.05), but this reduction was of negligible clinical importance and no longer statistically significant after limiting analyses to studies of longer duration or of higher quality. The frequency of adverse effects was low and, in clinical trials, indistinguishable from placebo. CONCLUSION: Treatment with milk thistle appears to be safe and well tolerated. We found no reduction in mortality, in improvements in histology at liver biopsy, or in biochemical markers of liver function among patients with chronic liver disease. Data are too limited to exclude a substantial benefit or harm of milk thistle on mortality, and also to support recommending this herbal compound for the treatment of liver disease.


    http://www.ncbi.nlm.nih.gov/pubmed/11481618
    Beneficial effects of silymarin on estrogen-induced cholestasis in the rat: a study in vivo and in isolated hepatocyte couplets.

    Crocenzi FA, Sanchez Pozzi EJ, Pellegrino JM, Favre CO, Rodriguez Garay EA, Mottino AD, Coleman R, Roma MG.

    Instituto de Fisiologia Experimental (IFISE)-Facultad de Ciencias Bioquimicas y Farmaceuticas (CONICET - U.N.R.), Rosario, Argentina.

    The effect of silymarin (SIL) on 17alpha-ethynylestradiol (EE)-induced cholestasis was evaluated in rats. EE (5 mg/kg, subcutaneously, daily, for 5 days) decreased both the bile-salt-dependent and the bile-salt-independent fractions of the bile flow. The decrease in the former was associated to a reduction in the bile salt pool size (-58%), and this effect was completely prevented by SIL. This compound also counteracted the inhibitory effect induced by EE on HCO(3)(-) but not glutathione output, 2 major determinants of the bile-salt-independent bile flow. EE decreased the secretory rate maximum (SRM) of tauroursodeoxycholate, (-71%) and bromosulfophthalein (BSP; -60%), as well as the expression of the BSP canalicular carrier, mrp2; SIL failed to increase mrp2 expression, and had only a marginal beneficial effect on both tauroursodeoxycholate and BSP SRM values. However, the two-compartment model-based kinetic constant for BSP canalicular transfer was significantly improved by SIL (+262%). SIL decreased rather than increased CYP3A4, the cytochrome P450 isoenzyme involved in the oxidative metabolism of EE, and had no inhibitory effect on the UDP-glucuronosyltrasferase isoforms involved in the formation of its 17beta-glucuronidated, more cholestatic metabolite. Pretreatment of isolated rat hepatocyte couplets with silibinin, the major, active component of SIL, counteracted the estradiol 17beta-glucuronide-induced decrease in the percentage of couplets secreting apically the fluorescent bile acid analogue, cholyl-lysyl-fluorescein. These results show that SIL protects against EE-induced cholestasis by normalizing mainly the decrease in the bile salt pool size and HCO(3)(-) output, and probably by counteracting the cholestatic effect of its cholestatic, glucuronidated metabolite.
    "The only way you can hurt the body is not use it. Inactivity is the killer and, remember, it's never too late."
    ~Jack Lalanne



  11. #11
    Super Moderator sassy69's Avatar
    Join Date
    Feb 2009
    Location
    Plate Junkie
    Posts
    10,633
    Rep Power
    2147943

    Default

    Not a promotion for either of these but just grabbing some of the product info about them as they are the most commonly referenced "products" for liver protection outside of just "milk thistle".

    Tyler's Liver Detox:

    TYLER DETOXIFICATION FACTORS Your liver possesses the remarkable capacity to detoxify hundreds of highly toxic chemicals to which your body is constantly exposed. Key nutrients must be present in certain amounts to keep your liver doing its job properly. When the liver is not working properly, there builds up a damaging accumulation of toxins which can lead to chronic degenerative disease. Tyler, a leader in the development of gastrointestinal & metabolic support products has developed a unique effective formulation, not manufactured elsewhere. Detoxification Factors supplies the nutritional precursors & co-factors essential for both Phase I & Phase II liver detoxification pathways. It provides antioxidants, conjugating agents, glutathione, glutathione precursors, sulfhydryl & methyl donors & vitamin & mineral co-factors.

    LIV-52:

    Liv-52 was introduced in 1955 by Himalaya Herbal Healthcare. Since then, it has been sold worldwide and is recognized by thousands of health professionals as one of the most effective liver formulas, with beneficial effects reported in over 300 studies on a variety of cases. Liv52 ensures optimum liver function through the protection of the hepatic parenchyma, and by way of its potent antioxidant properties. Liv-52 / LiverCare neutralizes all kind of toxins and poisons from food, water, air and medications, all sources of detrimental effects on the liver. Counteracting those hard to avoid poisons and protecting one of the body's most important organs. Alcohol users in partucular find Liv-52/LiverCare helpful in maintaining a healthier liver. It also helps those taking necessary allopathic medications to protect themselves against the damaging hepatoxic side effects.
    Liv-52 is a unique, all-natural, complex multi-ingredient formula. It is safe and effective in portecting the liver against harmful toxins from drugs, alcohol, food and water. Liv52 helps regulate levels of enzymes and optimizes assimilation. Liv-52 ( Liv52 ) has also been found to be associated with an increase in serum albumin, which is another indication of the liver protection it provides. Recent work shows that Liv52 has cholesterol-regulating action. Clinically, it helps maintain healthy levels of serum cholesterol, lipoproteins, phospholipids and triglycerides.

    Liv-52 restores the functional efficiency of the liver by protecting the hepatic parenchyma and promoting hepatocellular regeneration. The antiperoxidative activity of Liv-52 prevents the loss of functional integrity of the cell membrane, maintains cytochrome P-450, hastens the recovery period and ensures early restoration of hepatic functions in infective hepatitis. Liv-52 facilitates rapid elimination of acetaldehyde, the toxic intermediate metabolite of alcohol metabolism, and ensures protection from alcohol-induced hepatic damage. Liv-52 diminishes the lipotropic activity in chronic alcoholism, and prevents fatty infiltration of the liver. In pre-cirrhotic conditions, Liv-52 arrests the progress of the disease and prevents further liver damage

    Liv-52 Benefits

    Himalaya Liv-52 has a wide variety of benefits. Liv52 can be used in following conditions:

    Recent News about Liv-52

    In what is believed to be the first multi-herb remedy granted regulatory approval as a drug, Liv-52, the well-known hepatoprotective product of The Himalaya Herbal Healthcare, has recently been registered a safe and effective drug by the "Intercantonal Office for the Control of Medicines," Switzerland's equivalent of the United States' FDA. Read more at the following link - Himalaya's Liv-52 - LiverCare Approved as a Herbal Drug in Switzerland
    The ABC Clinical Guide to Herbs, published by the American Botanical Council (ABC): Liv-52 is one of 13 proprietary herbal formulas included in the publication's Clinical Studies/Proprietary Herbal Product Monograph section. Read more at the following link - Himalaya's Liv-52 - LiverCare - One of 13 Herbal Formulas Included in the ABC Clinical Guide to Herbs
    "The only way you can hurt the body is not use it. Inactivity is the killer and, remember, it's never too late."
    ~Jack Lalanne



  12. #12
    Super Moderator sassy69's Avatar
    Join Date
    Feb 2009
    Location
    Plate Junkie
    Posts
    10,633
    Rep Power
    2147943

    Default

    List of research studies and clinical trials on Liv-52

    Liv-52 by Himalaya is one of the most researched herbal products one can find. More than 300 clinical studies, many double-blind, placebo-controlled, have been performed on Liv-52 (LiverCare) since its introduction more than 47 years ago. Since then, it has become one of the most widely sold medications in the world with more than two billion tablets produced annually.
    In the prevention and treatment of viral hepatitis

    1. Evaluation of efficacy and safety of Liv.52 DS tablets in acute viral hepatitis: A prospective, double-blind, randomized, placebo-controlled, phase III clinical trial (pdf)
      Dr. Rajiv Baijal, M.D., D.N.B.1, Dr. Nikhil Patel, M.D.,2 and Dr. S. A. Kolhapure, M.D.3* 1Gastroenterologist, 2Research Associates, Department of Gastroenterology, Jagjivanram Western Railway Hospital, Mumbai Central, Mumbai, India, 3Senior Medical Advisor, R&D Center, The Himalaya Drug Company, Bangalore, India, Medicine Update 2004; 12(5), 41-53.
    2. Meta-analysis of 50 Phase III clinical trials in evaluation of efficacy and safety of Liv.52 in infective hepatitis (pdf)
      Kolhapure, S.A., M.D., Senior Medical Advisor, and Mitra, S.K., M.D., Executive Director,Research and Technical Service, R&D Center, The Himalaya Drug Company, Bangalore, India, Medicine Update (2004): 12(2), 51-61.
    3. Comparative efficacy of five indigenous compound formulations in patients of acute viral hepatitis (pdf)
      Dange, S.V., Lecturer, Patki, P.S., Reader, Pawar, S.S., Laboratory Technician, Phadke, S.A., Associate Professor and Shrotri, D.S., Professor and Head, Departments of Pharmacology and Microbiology, B.J. Medical College, Pune, India, Maharashtra Medical Journal (1989): (XXXVI), 5, 75.
    4. A trial with Liv.52 in infective hepatitis (pdf)
      Vijaykumar, S. Karchi, X-ray Unit, Talkoti, Karnataka, Capsule (1988): Feb./Mar.,126.
    5. A study of serum glycolytic enzymes and serum B hepatitis in relation to Liv.52 therapy (pdf)
      Patney, N.L. and Sumanbala Pachori, Postgraduate Department of Medicine, S.N. Medical College, Agra, Uttar Pradesh, The Medicine and Surgery (1986): (XXVI), 4, 9.
    6. Liv.52 in infective hepatitis including precoma and coma (pdf)
      Phadke, M.A. (Mrs.), Alka Datar and Nainesh M. Vora, B.J. Medical College and Sassoon General Hospitals, Pune, Maharashtra, Capsule (1984): (22), 8, 170.
    7. Studies with Liv.52 in the treatment of infective hepatitis, chronic active hepatitis and cirrhosis of the liver (pdf)
      Mandal, J.N. and Roy, B.K., Department of Medicine, Medical College and Hospital, Calcutta, West Bengal, Probe (1983): (XXII), 4, 217.
    8. Antiviral activity of plant extract Liv.52 in mice experimentally infected with Semliki forest encephalitis virus (pdf)
      Singh, V.K., George, C.X., Gupta, K.P. and Gupta, B.M., Central Drug Research Institute, Lucknow, Uttar Pradesh, Science and Culture (1983): 49, 354.
    9. Management of infective hepatitis (pdf)
      Sreenivasa Rao, Y., I.S.&W.P. Hospital, Jamshedpur, Bihar, Probe (1983): (XXII), 2, 107.
    10. Role of Liv.52 in the treatment of infective hepatitis (pdf)
      Chowdhury, A.B., Government Subdivisional Hospital, Karimganj, Cachar District, Assam, Capsule (1981): 3, 50.
    11. Infective hepatitis and Liv.52 drops (pdf)
      Dinesh Chandra Misra, Primary Health Centre, Marteengaj, Azamgarh, Uttar Pradesh, Capsule (1981): 6, 122.
    12. Liv.52 therapy in acute infective hepatitis (pdf)
      Kesarkar, A.S., S.V. Road, Goregaon West, Bombay, Maharashtra, Capsule (1981): 4, 74.
    13. Role of Liv.52 in the treatment of infective hepatitis (pdf)
      Paritosh Biswas, Ashoke Nagar, (24 Parganas), Alipur, West Bengal, Capsule (1980): 4, 74.
    14. Study of Liv.52 therapy in infective hepatitis in children (pdf)
      Shakuntala Saxena, (Mrs.), Ashok Kumar Garg and Ashok Jain, Department of Paediatrics, S.M.S. Medical College and Hospital, Jaipur, Rajasthan, Current Medical Practice (1980): (24), 5, 194.
    15. Viral hepatitis and Liv.52 (pdf)
      Uday Shankar Mandal, Giridih Block, Sirsia, Giridih, Bihar, Capsule (1980): 3, 50.
    16. Liv.52 in acute viral hepatitis – Results of a double-blind study (pdf)
      Habibullah, C.M., Vinod Chandra, Padmanaban, C.G. and Ramakrishna, R., Department of Gastroenterology, Osmania General Hospital, Hyderabad, Andhra Pradesh, The Antiseptic (1978): (75), 8, 491.
    17. Effect of an indigenous preparation Liv.52 on hepatitis B antigen-carriage (pdf)
      Kelkar, S.S., Grant Medical College, Bombay, Maharashtra, and Mahajan, R.K., Medical College, Aurangabad, Maharashtra, Probe (1978): (XVII), 2, 150.
    18. A preliminary report on the role of Liv.52, an indigenous drug in serum B hepatitis (Australia antigen positive) cases (pdf)
      Patney, N.L. and Ashok Kumar, Postgraduate Department of Medicine, S.N. Medical College, Agra, Uttar Pradesh, Probe (1978): (XVII), 2, 132.
    19. Clinical management of severe acute hepatic failure with special reference to Liv.52 therapy (pdf)
      Sethi, J.P. and Madhulika Sharma, Department of Medicine, S.M.S. Medical College and Hospital, Jaipur, Rajasthan, Probe (1978): (XVII), 2, 155.
    20. Liv.52 therapy in viral hepatitis (A clinico-biochemical study) (pdf)
      Banerjee, L.K., Sahu, N.N., Ray, S.S. and Daljit Singh, BSF Base Hospital, Kadamtala, Siliguri, Darjeeling, West Bengal, Capsule (1977): 8, 170.
    21. A clinical study of infective hepatitis treated with Liv.52 (pdf)
      Ila V. Desai, Dudhia, M.V. and Gandhi, V.K., Sheth K.M. School of Postgraduate Medicine and Research, and Sheth V.S. General Hospital and Smt. N.H.L. Municipal Medical College, Ahmedabad, Gujarat, Indian Paediatrics (1977): 3, 197.
    22. Observations on the treatment of infective hepatitis with an indigenous drug Liv.52 (pdf)
      Singh, K.K., Department of Medicine, Singh, Y.K., Sinha, S.K., Department of Paediatrics, Sharma, V., Department of Medicine and Mishra, B.N., Department of Medicine, Darbhanga Medical College, Laheriasarai, Bihar, Indian Medical Journal (1977): 5, 69.
    23. Clinical trial of Liv.52 drops in infective hepatitis – A comparative study with broad spectrum antibiotics and corticosteroids (pdf)
      Agrawal, V.K. and Meena Sareen, M.L.N. Medical College, Allahabad, Uttar Pradesh, Probe (1976): (XV), 2, 112.
    24. Viral hepatitis in children (pdf)
      Chawhan, R.N., Talib, S.H., Talib, V.H., Sengupta, S.R. and Patil, S.D., Medical College, Aurangabad, Uttar Pradesh, The Medicine and Surgery (1976): 3, 9.
    25. Efficacy of an indigenous compound preparation Liv.52 in acute viral hepatitis – A double-blind study (pdf)
      Sama, S.K., Krishnamurthy, L., Ramachandran, K. and Krishnan Lal, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, Indian Journal of Medical Research (1976): 5, 738.
    26. A study of chronic hepatitis in northern India (pdf)
      Singh, D.S., Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry, Sama, S.K., Sir Ganga Ram Hospital, New Delhi and Singh, G., Department of Gastroenterology, All India Institute of Medical Sciences, New Delhi, Indian Journal of Medical Research (1976): (64), 12,1728.
    27. Viral hepatitis in children (pdf)
      Reddi, Y.R., Sudhakar Rao, V., Rohini, K. and Kusuma, G., Institute of Child Health, Niloufer Hospital, Hyderabad, Andhra Pradesh, Indian Paediatrics (1975): (XII), 8, 659.
    28. Studies on Liv.52 in hepatic disorders – Part II (pdf)
      Sharma, N.L., Lahori, U.C. and Mehta, S.K., King George Medical College, Lucknow, Uttar Pradesh, Probe (1975): (XIV), 2, 126.
    29. Liv.52 in infective hepatitis (pdf)
      Bhandari, N.R. and Shashi Gupta (Miss.), Department of Paediatrics, Gandhi Medical College, Bhopal, Madhya Pradesh, Probe (1974): (XIV), 1, 68.
    30. Acute infectious hepatitis with fulminant hepatic failure – A study of 289 cases (pdf)
      Deshpande, R.S., Kasturba Hospital for Infectious Diseases, Sane Guruji Marg, Bombay, Maharashtra, Probe (1974): (XIV), 1, 1.
    31. Trial of Liv.52 in infectious hepatitis in children in Goa (pdf)
      Harish Mazumdar and Mira Mazumdar, Department of Paediatrics, Goa Medical College, Panaji, Goa, Probe (1974): (XIV), 1, 28.
    32. Studies with Liv.52 in infective hepatitis (pdf)
      Jain, K.C., Khanijo, S.K. and Bisarya, B.N., Department of Medicine, S.S. Medical College, Rewa, Madhya Pradesh, Probe (1974): (XIV), 1, 64.
    33. Liv.52 therapy in infective hepatitis (pdf)
      Khetarpal, S.K. and Veera Kumar, E., Department of Paediatrics, Medical College, Amritsar, Punjab, Probe (1974): (XIV), 1, 59.
    34. Trial of Liv.52 in infectious hepatitis in children in Goa (pdf)
      Mazumdar, H. and Mazumdar, M., Department of Paediatrics, Goa Medical College, Panaji, Goa, Probe (1974): (XIV), 1, 82.
    35. Liv.52 in viral hepatitis with special reference to its use in precoma and coma (pdf)
      Mitra, D.K., Ashrafuddin, S. and Talib, S.H., Department of Medicine, Medical College, Aurangabad, Maharashtra, Probe (1974): (XIV), 1, 14.
    36. Role of Liv.52 and steroids in the management of viral hepatitis in children (pdf)
      Reddi, Y.R., Rohini, K., Kusuma, G. and Sudhakar Rao, V., Osmania Medical College, Institute of Child Health and Niloufer Hospital, Hyderabad, Andhra Pradesh, Probe (1974): (XIV), 1, 35.
    37. Studies on Liv.52 in hepatic disorders – Part I (pdf)
      Sharma, N.L., Lahori, U.C. and Mehta, S.K., King George Medical College, Lucknow, Uttar Pradesh, Probe (1974): (XIV), 1, 54.
    38. Observations on the therapy of acute infectious hepatitis with Liv.52 (pdf)
      Shishupal Ram and Kumar, P., Liver Research Unit, Hospital for Children, Patna Medical College Hospital, Patna, Bihar, Probe (1974): (XIV), 1, 66.
    39. Studies on 222 cases of acute infective hepatitis during an epidemic (pdf)
      Sinha, B.B., Kurzi Holy Family Hospital, Patna, Bihar, Probe (1974): (XIII), 3, 130.
    40. Liv.52 trial in infective hepatitis (pdf)
      Mehrotra, M.P.,and Dineshchandra Mathur, Research Fellow, S.N. Medical College, Agra, Uttar Pradesh, The Antiseptic (1973): (70), 2, 114.
    41. Liv.52 in the treatment of acute infective hepatitis (pdf)
      Sarkar, M.K., Burn and Co., Durgapur, Burdwan, Rajasthan, The Indian Practitioner (1973): 8, 395.
    42. Clinico-biochemical study of infective hepatitis with special reference to Liv.52 therapy (pdf)
      Dave, D.S., Rajput, V.J. and Gupta, M.R., Department of Paediatrics, G.R. Medical College, Gwalior, Madhya Pradesh, Probe (1972): (XI), 4, 214.
    43. Therapeutic effects of Liv.52 in post-necrotic hepatitis (pdf)
      Gupta, S., Khatri, R.L. and Srivastava, G., Maulana Azad Medical College, New Delhi, Probe (1972): (XII), 1, 15.
    44. Therapy of infectious hepatitis and other liver disorders (pdf)
      Gupta, S., Khatri, R.L. and Srivastava, G., Maulana Azad Medical College, New Delhi, Probe (1972): (XI), 2, 93.
    45. Liv.52 therapy in viral hepatitis (pdf)
      Patel, G.T., Mruthyunjayanna, B.P., Seetharam, T.D. and Channe Gowda, A.C., Medicine Unit, Victoria Hospital and Bangalore Medical College, Bangalore, Karnataka, Probe (1972): (XI), 2, 112.
    46. Chronic active hepatitis (A preliminary observation of 10 cases) (pdf)
      Dasgupta, M. and Mukerjee, A.B., Department of Medicine, R.K. Mission Seva Pratisthan, Calcutta, West Bengal, Journal of Indian Medical Profession (1971): 18, 8097.
    47. Infectious hepatitis – Study of 100 cases (pdf)
      Deshpande, R.S., Kasturba City Fever Hospital, Bombay, Maharashtra, Shantilal C. Sheth, Kasturba City Fever Hospital and Emeritus Director Professor of Paediatrics, Topiwala National Medical College and Nair Hospital, Bombay, Maharashtra, and Joy Kutty, M.D., Research Scholar, Bombay, Maharashtra, Current Medical Practice (1971): 6, 810.
    48. Some observations on Liv.52 in the treatment of infective hepatitis and cirrhosis of liver (pdf)
      Lala Surajnandan Prasad, Department of Paediatrics, Patna University, and Kaleshwer Prasad, Department of Paediatrics, Children’s Hospital, Patna Medical College and Hospital, Patna, Bihar, Probe (1971): (X), 3, 114.
    49. Liv.52 studies in acute hepatitis (pdf)
      Ramalingam, V., Sundarvalli, N. and Balagopal Raju, V., Institute of Child Health and Hospital for Children, Egmore, Madras, Tamil Nadu, Indian Paediatrics (1971): 12, 839.
    50. Infective hepatitis – Survey and study of 110 cases (pdf)
      Doddagoudar, M.B., Karnatak Medical College, Hubli, Karnataka, Probe (1970): (IX), 3, 122.
    51. Treatment of viral hepatitis by an indigenous drug – Liv.52 (pdf)
      Mukerjee, A.B., Calcutta National Medical College and Hospitals, and Department of Medicine,Dasgupta, M., Ramakrishna Mission Seva Pratishthan, Calcutta, West Bengal, The Indian Practitioner (1970): June, 357.
    52. Liv.52 in infective hepatitis (pdf)
      Jaffari, S.M.H. and Shyam Raj, Fever Hospital, Hyderabad, Andhra Pradesh, The Antiseptic (1969): 5, 353.
    53. Role of various types of treatment in infectious hepatitis (pdf)
      Major Arora, J.K., MH Lebong, Darjeeling, West Bengal, Armed Forces Medical Journal (1969): (XXV), 3, 362.
    54. Studies with Liv.52 therapy in infective hepatitis (pdf)
      Sule, C.R., Pai, V.R., Damania, R.F. and Joshi, V.S. (Miss.), Medicine Unit, Sasoon General Hospitals and B.J. Medical College, Poona, Maharashtra, Journal of Indian Medical Profession (1968): 14, 6391.
    55. Preliminary observations on the role of Liv.52 in infective-hepatitis with persistent jaundice (pdf)
      Rath, B.B., Department of Medicine, Sengupta, S.N., Department of Medicine, and Bose, S.N., Department of Biochemistry, Bankura Sammilani Medical College and Hospital, Bankura, West Bengal, Capsule (Undated): (XV), 8, 170.
    In the prevention and treatment of alcoholic liver disease

    1. Role of Liv.52 - A herbal formulation on 14C-Ethanol metabolism and 14C-Acetaldehyde accumulation in rat liver (pdf)
      Singh, B., Department of Nuclear Medicine, PGIMER, Chandigarh, Punjab, and Dhawan, D., Department of Biophysics, Panjab University, Chandigarh, Punjab, Indian Journal of Nuclear Medicine (2000): (15), 1, 27.
    2. Hepatoprotective effects of Liv.52 on ethanol-induced liver damage in rats (pdf)
      Rajat Sandhir and Gill, K.D., Department of Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh, Haryana, Indian Journal of Experimental Biology (1999): (37), August, 762.
    3. Effect of the hepatoprotective drug Liv.52 on liver damage (pdf)
      M. Kalab, T. Krechler Internal Clinic of the Medical Faculty of the Charles University in Prague and The Military Faculty Hospital in Prague, The Journal of Czech Physicians (1997): (136), 24, 758-760.
    4. Bioassay for evaluation of the hepatoprotective effect of Liv.52, a polyherbal formulation, on ethanol metabolism in chronic alcohol – Exposed rats (pdf)
      Chauhan, B.L., Mohan, A.R., Kulkarni, R.D. and Mitra, S.K., R&D Centre, The Himalaya Drug Co., Bangalore, Karnataka, Indian Journal of Pharmacology (1994): (26), 117.
    5. Protective effect of Liv.52 on alcohol-induced fetotoxicity (pdf)
      Gopumadhavan, S., Jagadeesh, S., Chauhan, B.L. and Kulkarni, R.D., R&D Centre, The Himalaya Drug Co., Bangalore, Karnataka, Alcoholism: Clinical and Experimental Research (1993): (17), 5, 1089.
    6. Alcoholic liver disease – The possibility of ayurvedic therapy (pdf)
      Kulkarni, R.D., Clinical Pharmacology, Bombay, Maharashtra, The Journal of General Medicine (1992): (4), 2, 11.
    7. Alcohol hangover and Liv.52 (pdf)
      Chauhan, B.L. and Kulkarni, R.D., R&D Centre, The Himalaya Drug Co., Bombay, Maharashtra, European Journal of Clinical Pharmacology (1991): 40, 187.
    8. Effect of Liv.52, a herbal preparation, on absorption and metabolism of ethanol in humans (pdf)
      Chauhan, B.L. and Kulkarni, R.D., R&D Centre, The Himalaya Drug Co., Bombay, Maharashtra, European Journal of Clinical Pharmacology (1991): 40, 189.
    9. Dose response of ethanol after chronic administration of alcohol and effect of Liv.52 on blood, liver ethanol and acetaldehyde levels in rats (pdf)
      Chauhan, B.L. and Kulkarni, R.D., R&D Centre, The Himalaya Drug Co., Bombay, Maharashtra, European Journal of Pharmacology (1990): (183), 5, 1864.
    10. Blood, urine ethanol and acetaldehyde levels from six different alcoholic beverages and effect of Liv.52 (pdf)
      Kulkarni, R.D. and Chauhan, B.L., R&D Centre, The Himalaya Drug Co., Bombay, Maharashtra, European Journal of Pharmacology (1990): (183), 5, 1865.
    11. Addiction and industry (pdf)
      Alan De Sousa, J.J. Hospital and Grant Medical College, Bombay, Maharashtra, Industrial Psychiatry Journal (1989): 2, 1, 5.
    12. Liv.52 in alcoholism (pdf)
      Alan De Souza, Prakash Gangdev, Ashok Sinorawala and Manoj Agrawal, Department of Psychiatry, Grant Medical College and J.J. Hospital, Bombay, Maharashtra, Journal of Communication Psychiatry (1989): (12), Jan./Mar., 23.
    13. Injurious effects of ethyl alcohol on liver function and protective effect of Liv.52 (pdf)
      Doshi, B.S. and Kulkarni, R.D., The Indian Practitioner (1987): Nov., 965.
    14. The mechanism of cellular damage in alcoholic liver disease and the protective action of Liv.52 (pdf)
      Soman, R.N., Bhatia General Hospital, Tardeo, Bombay, Maharashtra, Probe (1983): (XXII), 3, 164.
    15. Effect of ethanol on liver function and its relation to hangover: Protective effect of Liv.52 (pdf)
      Kulkarni, R.D., Grant Medical College, Bombay, Maharashtra, Indian Drugs (1980): 11, 363.
    16. Electron microscopic study of the liver after prolonged use of alcohol (pdf)
      Prasad, G.C., Department of Shalya Shalakya and Surgical Research Laboratory, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, Probe (1980): (XIX), 3, 179.
    17. Effect of Liv.52 on different bio-chemical parameters in alcoholic cirrhosis (pdf)
      Dubey, G.P., Aruna Agrawal and Dixit, S.P., Department of Basic Principles, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, The Antiseptic (1977): (91), 6, 205.
    18. Effect of an indigenous drug Liv.52 against alcohol-induced hepatic damage – A biochemical study (pdf)
      Subbarao, V.V., Department of Physiology and Biochemistry, S.N. Medical College, Jodhpur, Rajasthan, Probe (1976): (XV), 4, 235.
    19. Prolonged moderate alcohol intake and liver function (pdf)
      Damle, V.B., L.T.M.G. Hospital and L.T.M. College, Sion, and Kulkarni, R.D., Grant Medical College and J.J. Group of Hospitals, Bombay, Maharashtra, Probe (1973): (XIII), 1, 31.
    20. Effect of Liv.52 on growth and alcohol-induced hepatic dysfunction in rats (pdf)
      Kale, A.K., Kulkarni, S.D. (Mrs.), Joglekar, G.V. and Balwani, J.H., B.J. Medical College, Poona, Maharashtra, Current Medical Practice (1966): (10), 240.
    In the prevention and treatment of pre-cirrhotic conditions and early cirrhosis

    1. The efficacy of Liv-52 on liver cirrhotic patients: A randomized, double-blind, placebo-controlled first approach (pdf)
      H. Fallah Huseinia*, S.M. Alavianb, R. Heshmatc, M.R. Heydarid, K. Abolmaalie a Department of Pharmacology, Institute of Medicinal Plants, No. 97, Bozorgmehr St., Ghods St., Enghelab Ave., Tehran, Iran. b Baqiatallah University of Medical Sciences, Tehran Hepatitis Center, Tehran, Iran. c Department of Epidemiology and Biostatistics, Tehran University of Medical Sciences, Tehran, Iran. d Endocrinology & Metabolism Research Center, Tehran University of Medical Sciences, Tehran, Iran. e Baqiatallah University of Medical Sciences, Tehran, Iran Phytomedicine 12(2005) 619-624.
    2. A novel mechanism of action prevents ethanol-induced injury – Liv.52 profile of an herbal remedy (pdf)
      Chauhan, B.L. and Kulkarni, R.D., R&D Centre, The Himalaya Drug Co., Bangalore, Karnataka, Drug News & Perspectives (1993): (6), 9, 662.
    3. Liv.52 in the management of various hepatic disorders – A study of 53 cases (pdf)
      Bharadia, G.R., Kukade, A.L., Kulkarni, A.S. and Rathod, I.M., Vivekanand Hospital, Latur, Maharastra, Probe (1986): (XXV), 3, 277.
    4. Role of Liv.52 in Indian childhood cirrhosis, with special reference to its effect on alpha-I-antitrypsin levels (pdf)
      Nawal Kishore Agrawal, Prasad, R., Manju Sharma and Sharma, B.B., S.N. Medical College and Hospital, Agra, Uttar Pradesh, Asian Medical Journal (1982): 9, 647.
    5. Role of Liv.52 in management of Indian childhood cirrhosis (pdf)
      Shakuntala Saxena (Mrs.), Ashok Kumar Garg and Ashok Jain, Department of Paediatrics, S.M.S. Medical College and Hospital, Jaipur, Rajasthan, Current Medical Practice. (1980): (24), 7, 269.
    6. Role of Liv.52 in hepatic and cirrhosis of the liver (pdf)
      Mallik K.K. and Pal, M.B., Department of Medicine, Institute of Postgraduate Medical Education and Research, Calcutta, West Bengal, Current Medical Practice (1979): 23, 5.
    7. Liv.52 in the treatment of cirrhosis of liver – Certain observations (pdf)
      Singh, K.K., Department of Medicine, Singh, Y.K., Dubey, K.M., Department of Biochemistry, Sharma, V., Department of Medicine, and Mishra, B.N., Darbhanga Medical College, Laheriasarai, Bihar, The Antiseptic (1979): (76), 7, 393.
    8. A study of therapeutic actions of Liv.52 on various stages, severity, and activity of portal cirrhosis and infective hepatitis (pdf)
      Sinha, P.K., B.R.D. Medical College, Gorakhpur, Uttar Pradesh, Ashok Kumar and Patney, N.L., Post-graduate Department of Medicine, S.N. Medical College, Uttar Pradesh, Probe (1979): (XVIII), 3, 157.
    9. Study of Liv.52 therapy in cases of Indian childhood cirrhosis and other liver disorders (pdf)
      Mehar Singh and Agrawal, V.K., S.N. Children’s Hospital, M.L.N. Medical College, Allahabad, Uttar Pradesh, Probe (1978): (XVII), 2, 169.
    10. Management of steatorrhoea of cirrhosis of the liver by an indigenous drug – Liv.52 (pdf)
      Patney, N.L., Jasuja, R.K. and Ashok Kumar, Postgraduate Department of Medicine, S.N. Medical College, Agra, Uttar Pradesh, Probe (1976): (XV), 3, 164.
    11. Liv.52 – A clinico-biochemical trial in hepatic cirrhosis (pdf)
      Mehrotra, M.P. and Tandan, S., S.N. Medical College, Agra, Uttar Pradesh, Current Medical Practice (1973): (17), 4, 185.
    12. Hepatic cirrhosis in the tropics (pdf)
      Mukerjee, A.B., Calcutta National Medical College and Hospital, Calcutta, West Bengal, Dasgupta, M., Resident University of Tennessee College of Medicine, USA, and Sarkar, S.K., N R Sarkar Medical College, Calcutta, West Bengal, Probe (1973): (XII), 2, 91.
    13. Liv.52 – A new therapeutic agent in the management of steatorrhoea of cirrhosis of the liver (pdf)
      Patney, N.L., Jasuja, R.K. and Ashok Kumar, Postgraduate Department of Medicine, S.N. Medical College, Agra, Uttar Pradesh, Journal of Research in Indian Medicine (1973): 3, 28.
    14. Long-term studies on the therapy of hepatic damage and cirrhosis of liver (pdf)
      Lala Surajnandan Prasad, Patna Medical College and Prince of Wales Hospital, Patna, Bihar Sinha, K.N., Prince of Wales Hospital, Patna, Bihar, Devendra Tripathy and Prasad, K., Research Scholar, Patna, Bihar, Current Medical Practice (1971): (15), 12, 1071.
    15. Cirrhosis of liver – Results of treatment with an indigenous drug: Liv.52 (pdf)
      Mukerjee, A.B. and Dasgupta, M., Department of Medicine, Ramakrishna Mission Seva Pratishthan, Calcutta, West Bengal, Journal of Indian Medical Profession (1971): 17, 7853.
    16. B.S.P. test in the evaluation of therapy in hepatic cirrhosis by an indigenous drug – Liv.52 (pdf)
      Dasgupta, M., Ramakrishna Mission Seva Pratishthan, Calcutta, West Bengal,and Mukerjee, A.B., Calcutta National Medical College and Hospitals, Calcutta, West Bengal, The Indian Practitioner (1970): 12, 739.
    17. Cirrhosis of liver (pdf)
      Shantilal C. Sheth and Tibrewala, N.S., Bharat Medical Journal (1970): (2), 2, 130.
    18. Liv.52 – Infantile cirrhosis (pdf)
      Paulose, P.M., The Indian Practitioner (1963): 6, 516.
    19. Clinical and histopathological evaluation of Liv.52 in cirrhosis in liver (pdf)
      Vyas, K.J., General Hospital, Junagadh, Gujarat, Probe (1963): 2, 66.
    20. Treatment of hepatopathy in children with a combination of capparis spinosa and other Indian indigenous drugs (pdf)
      Vyas, K.J., Children Ward, General Hospital, Junagadh, Gujarat, Medical Digest (1961): (29), 3, 105.
    21. Therapy of cirrhosis of liver and liver damage with indigenous drugs – Experimental and clinical studies (pdf)
      Shantilal C. Sheth, Basil J. Northover, Tibrewala, N.S., Warerkar, U.R. and Karande, V.S. B.Y.L. Nair Hosptial and Topiwala National Medical College and the Christian Medical College and Hospital, Vellore, Tamil Nadu, Indian Journal of Paediatrics (1960): 27, 204.
    22. Liv.52 therapy in cirrhosis of liver in children (pdf)
      Vyas, K.J., Indian Journal of Child Health (1960): 5, 244.
    23. Treatment of infantile cirrhosis with an indigenous preparation (pdf)
      Vyas, K.J., Children Hospital, Sir T. Hospital, Bhavnagar, Gujarat, The Indian Practitioner (1958): (XI), 1, 107.
    24. Some clinical observations on the use of Liv.52 (An indigenous drug) in cases of cirrhosis of liver in children (pdf)
      Mathur, P.S., Hamidia Hospital, Bhopal, Madhya Pradesh, Current Medical Practice (1957): 5, 107.
    In the prevention and treatment of protein energy malnutrition

    1. Malnourished children and Liv.52 (pdf)
      Renu Patel and Pereira, L., Department of Paediatrics, J.J. Group of Hospitals, Bombay, Maharashtra, The Indian Practitioner (1993): (XLVI), 7, 523.
    2. A study of the effect of Liv.52 syrup on malnourished children in rural area (pdf)
      Syed Fiaz Peeran, District Health Officer, Madurai District, Manivasagam, M. and Unnamalai, R., Primary Health Centre, Ammayanaickanur, Madurai District, Tamil Nadu, Capsule (1982): 4, 74.
    3. Effect of Liv.52 therapy in malnourished children (pdf)
      Shakuntala Saxena, (Mrs.), Ashok Kumar Garg and Ashok Jain, Department of Paediatrics, S.M.S. Medical College and Hospital, Jaipur, Rajasthan, Current Medical Practice (1980): 6, 229.
    4. Role of Liv.52 in children with malnutrition (pdf)
      Phadke, M.A. (Mrs.), Arkadi, D.P., Sainani, G.S., Upgraded Department of Medicine, and Phadke, M.V., Department of Medicine and Department of Paediatrics, B.J. Medical College and Sassoon General Hospitals, Pune, Maharashtra, Probe (1978): (XVII), 2, 160.
    5. A study of the growth-promoting effect of Liv.52 in malnutrition (A clinical trial) (pdf)
      Shrivastava, D.K., Singwekar, A.G., Thawaani, Y.P. and Tiwari, A.K., Department of Child Health, G.R. Medical College and K.R. Hospital, Gwalior, Madhya Pradesh, Probe (1978): (XVII), 4, 305.
    6. Role of Liv.52 in the treatment of malabsorption syndrome (pdf)
      Tripathi, S.N., Misra, A.K., Upadhyaya, K.N., Dixit, O.P. and Srivastava, S.K., Department of Kayachikitsa, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, Journal of Research in Indian Medicine, Yoga and Homeopathy (1977): 1, 49.
    7. Management of protein-calorie malnutrition with Liv.52 as an adjuvant (pdf)
      Bhandari, B., R.N.T. Medical College and General Hospital, Udaipur, Rajasthan, Probe (1976): (XV), 4, 245.
    8. Liv.52 in sub-optimal growth (pdf)
      Desai, A.B. and Shah, A.A., Department of Paediatrics, B.J. Medical College, Ahmedabad, Gujarat, Probe (1976): (XV), 4, 247.
    9. A clinical study of the effect of Liv.52 on the growth pattern of normal and malnourished children in a rural area – 310 cases (pdf)
      Reddy, Y.R., Sulochana, K.S. and Mathur, Y.C., Niloufer Hospital, Hyderabad, Andhra Pradesh, Paediatric Clinics of India (1975): 3, 157.
    10. Liv.52 therapy in cases of malnutrition, infective hepatitis, infantile cirrhosis and anorexia (A clinico-pathological study) (pdf)
      Dayal, R.S., Kalra, K., Mital, V.P. and Rajiv Sharan, S.N. Medical College, Agra, Uttar Pradesh, The Antiseptic (1974): (71), 2, 89.
    11. Liv.52 in malnutrition and sub-optimal growth (pdf)
      Desai, A.B. (Mrs.), B.J. Medical College and Civil Hospital, Ahmedabad, Gujarat, Probe (1974): (XIII), 4, 167.
    12. Clinico-biochemical trials with an indigenous drug: Liv.52 – In malnutrition (pdf)
      Mathur, P.S., Chandra, I. and Khan, M.A., Department of Paediatrics, M.G.M. Medical College, Indore, Madhya Pradesh, Probe (1974): (XIII), 3, 136.
    13. Clinical evaluation of Liv.52 therapy in malnutrition during infancy and childhood (pdf)
      Dave, D.S., Rajput, V.J., Gupta, M.R., Jain, V.K. and Lavangikar, U. (Miss.), Department of Paediatrics, G.R. Medical College, Gwalior, Madhya Pradesh, Probe (1973): (XIII), 1, 1.
    14. Clinical trial of Liv.52 drops (pdf)
      Mangalam, S. and Sunderavalli, N., Government Royapettah Hospital, Bombay, Maharashtra, Mediscope (1973): (XVI), 1, 23.
    15. The effect of Liv.52 on the pattern of weight-gain in children with marasmus and other degrees of malnutrition as compared with that of non-virilizing androgens (pdf)
      Tirumala Rao, P., Aziz Mohd. Khan and Anjaiah, K., Department of Paediatrics, Gandhi Hospital, Secunderabad, Andhra Pradesh, Probe (1973): (XII), 2, 78.
    16. Malnutrition – Hepatic function and Liv.52 therapy (pdf)
      Khetarpal, S.K., Leela Ramkumar and Ram Lubhaya, Department of Paediatrics, Medical College, Patiala, Punjab, Current Medical Practice (1972): (16), 11, 481.
    17. Comparative trial of Liv.52 and orabolin in marasmus (pdf)
      Tirumala Rao, P., Aziz Mohd. Khan and Anjaiah, K., Secunderabad, Andhra Pradesh, Indian Journal of Paediatrics (1972): (39), 227.
    18. Liv.52 therapy in hypoproteinaemia (pdf)
      Vasant R. Pai, Borgave, M.A., Sule, C.R., Kale, S.S. and Sudam Kale, Department of Medicine, B.J. Medical College, Sassoon Hospitals, Poona, Maharashtra, Journal of Indian Medical Profession (1972): 6, 8447.
    19. A clinico-pathological study of hepatomegaly with special reference to Liv.52 therapy (pdf)
      Dayal, R.S., Kalra, K., Rajvanshi, V.S. and Baheti, P.C., S.N. Medical College, Agra, Uttar Pradesh, Journal of Indian Medical Profession (1970): (17), 9, 7768.
    20. Effect of Liv.52 on growing rats under the influence of corticosteroids (pdf)
      Kulkarni, S.D. and Joglekar, G.V., Department of Pharmacology, B.J. Medical College, Poona, Maharashtra, The Indian Practitioner (1970): 5, 299.
    In the prevention and treatment of loss of appetite

    1. Effect of Liv.52 on fenfluramine-induced anorexia (pdf)
      Gokhale, M.S., R&D Centre, The Himalaya Drug Co., Bombay, Maharashtra, Probe (1990): (XXIX), 3, 186.
    2. Liv.52 in anorexia of varying aetiology (pdf)
      Dharmalingam, A. and Chandrasekaran, K., Bhavani, Periyar District, Tamilnadu, Probe (1985): (XXIV), 4, 233.
    3. Liv.52 in post-cholecystectomy dyspepsia (pdf)
      Misgar, M.S., Karihaloo, Mir Nazir Ahmed, Sethi, S.K. and Mohd. Yousuf Wani, Department of Surgery, Government Medical College, Srinagar, Jammu and Kashmir, Probe (1984): (XXIII), 3, 150.
    4. Infant feeding problems and the role of Liv.52 (pdf)
      Dharam B. Sharma and Lahori, U.C., Children’s Hospital, Medical College, Jammu, Jammu and Kashmir, Probe (1980): 4, 275.
    5. Biological rhythms and medicine (pdf)
      Kulkarni, R.D., Grant Medical College, Bombay, Maharashtra, Current Medical Practice (1980): (24), 8, 305.
    6. The anabolic activity of Liv.52 (pdf)
      Aslam, M. and Aslam, S., Department of Obstetrician and Gynaecology, Jawaharlal Nehru Medical College, Aligarh Muslim University, Aligarh, Uttar Pradesh, Probe (1979): (XVIII), 2, 74.
    7. Effect of Liv.52 on anorexia of varied aetiology (pdf)
      Anil Mohan and Reddy S.V.R., Institute of Paediatrics and Child Health, Andhra Medical College, Visakhapatnam, Andhra Pradesh, Probe (1975): (XIV), 2, 136.
    8. Observation on the anabolic effects of Liv.52 in burns (pdf)
      Sinha, R.N., Singh, Y. and Madan, P., Department of Plastic Surgery, Patna Medical College Hospitals, Patna, Bihar, Indian Journal of Plastic Surgery (1972): (5), 1, 26.
    9. Effect of Liv.52 in anorexia of hookworm disease (A preliminary study) (pdf)
      Dutta, J.K., Balak Ram Hospital, Delhi, Probe (1971): (XI), 1, 26.
    10. Liv.52 in anorexia in paediatric practice (pdf)
      Saxena, S., S.M.S. Medical College, Jaipur, Rajasthan, Current Medical Practice (1971): 15, 580.
    11. Liv.52 in anorexia in children (pdf)
      Sesha Chari, K.R., Kakatiya Medical College, Warangal, Andhra Pradesh, Bharat Medical Journal (1971): 2, 181.
    12. Study on Liv.52 – An indigenous anabolic compound (pdf)
      Sunita D. Kulkarni, Kulkarni, D.S., Vasantgadkar, P.S. and Joglekar, G.V., Department of Pharmacology, Physiology and Anatomy, B.J. Medical College, Poona, Maharashtra, The Indian Practitioner (1971): 2, 145.
    13. Therapy of anorexia with Liv.52 (pdf)
      Indira Bai, K., Mallikarjuna Rao, V.P.R. and Subba Rao, K.V., S.V. Medical College, and S.V.R.R. Hospital, Tirupati, Andhra Pradesh, The Antiseptic (1970): 67, 615.
    14. Treatment of anorexia by Liv.52 (pdf)
      Mukherji, J.P., Moti Lal Nehru Hospital, Jabalpur Cantonment, Madhya Pradesh, Probe (1969): (IX), 1, 25.
    15. Mechanism of anorexia and effect of Liv.52 on food intake (pdf)
      Athavale, V.B., Lokmanya Tilak Municipal General Hospital, Sion, Bombay, Maharashtra, Probe (1966): 6, 12.
    16. Anabolic effect of Liv.52 (pdf)
      Damle, V.B. and Deshpande, K.J., Bombay, Maharashtra, Port Trust, Bombay, Maharashtra, The Indian Practitioner (1966): 19, 357.
    17. Therapy of anorexia with Liv.52 (pdf)
      Shantilal C. Sheth, Tibrewala, N.S., Warerkar, U.R. and Karande, V.S., B.Y.L. Nair Hospital and Topiwala National Medical College, Bombay, Maharashtra, Probe (1963): 4, 137.
    In the prevention and treatment of radiation and chemotherapy-induced liver damage

    1. Hepatoprotective effect of Liv.52 and kumaryasava on carbon tetrachloride-induced hepatic damage in rats (pdf)
      Meena Kataria and Singh, L.N., Division of Biochemistry and Food Science, Indian Veterinary Research Institute, Izatnagar, Uttar Pradesh, Indian Journal of Experimental Biology (1997): (35), June, 655.
    2. Protective effect of Liv.52 and Liv.100, ayurvedic formulations on lipid peroxidation in rat liver homogenate – An in vitro study (pdf)
      Suja, V., Latha Sharmila, S. and Shyamala Devi, C.S., Department of Biochemistry, University of Madras, Tamil Nadu, Guindy Campus, Madras, Tamil Nadu, Indian Journal of Experimental Biology (1997): (35), Jan., 50.
    "The only way you can hurt the body is not use it. Inactivity is the killer and, remember, it's never too late."
    ~Jack Lalanne



  13. #13
    Super Moderator sassy69's Avatar
    Join Date
    Feb 2009
    Location
    Plate Junkie
    Posts
    10,633
    Rep Power
    2147943

    Default

    1. Prevention of mercuric chloride-induced cerebellar damage in mice with a multiherbal hepatic drug results and possibilities (pdf)
      Varghese, J., Shrilakshmi, K. and Rathore, H.S., School of Studies in Zoology and Chemistry, Vikram University, Ujjain, Madhya Pradesh, Indian Journal of Occupational Health (1997): (40), 1, 1.
    2. Radioresponse of leucocytes in peripheral blood of mice against gamma irradiation and their protection by Liv.52 (pdf)
      Daga, S.S., Jain, V.K. and Goyal, P.K., Department of Zoology, University of Rajasthan, Jaipur, Rajasthan, Rajasthan, Probe (1995): (XXXIV), 3, 222.
    3. Liv.52 pretreatment inhibits the radiation-induced lipid peroxidation in mouse liver (pdf)
      Ganapathi, N.G. and Ganesh Chandra Jagetia, Department of Radiobiology, Kasturba Medical College, Manipal, Karnataka, Current Science (1995): (69), 7, 601.
    4. Hepatoprotective effects of Liv.52 and its indirect influence on the regulation of thyroid hormones in rat liver toxicity-induced by carbon tetrachloride (pdf)
      Dhawan, D. and Goel, A., Department of Biophysics, Punjab University, Chandigarh, Punjab, Research in Experimental Medicine (1994): 194, 203.
    5. Hepatoprotective role of Liv.52 in toxic conditions of Liver – An ultrastructural study (pdf)
      Dhawan, D., Goel, A. and Sharma, M.L., Department of Biophysics, Punjab University, Chandigarh, Haryana, IECM (1994): 17-22, 1243.
    6. Herbomineral preparations as adjuvants to chemotherapy in cancer breast (pdf)
      Durgesh Kumar Acharya, M.K.C.G. Medical College and Hospital, Berhampur, Ganjam, Orissa, The Antiseptic (1994): (91), 2, 67.
    7. Protection of fish liver with Liv.52 against cadmium intoxication – A histological study (pdf)
      Rathore, H.S. and Naik, B.K., School of Studies of Zoology, Vikram University, Ujjain, Madhya Pradesh, Biologia (Lahore) (1994): (40), 1 and 2, 1.
    8. Down regulation of tumour necrosis factor activity in experimental hepatitis by a herbal formulation, Liv.52 (pdf)
      Roy, A., Soni, G.R., Kolhapure, R.M., National Institute of Virology, Pune, Maharashtra, and Karnik, U.R. and Patki, P.S., Departments of Pathology and Pharmacology, B.J. Medical College, Pune, Maharashtra, Indian Journal of Experimental Biology (1994): 32, 694.
    9. Hepatoprotective effect of Liv.52 against CCl4-induced lipid peroxidation in liver of rats (pdf)
      Shivani Pandey, Gujrati, V.R., Shanker, K., Singh, N and Dhawan, K.N., Department of Pharmacology, K.G. Medical College, Lucknow, Uttar Pradesh, Indian Journal of Experimental Biology (1994): (32), Sep. 674.
    10. Protective effect of Liv.52 against anti-cancer chemotherapy in rats (pdf)
      Yadav, S. and Yadav, R.,Department of Anatomy and Biochemistry, Indira Gandhi Medical College, Shimla, Jammu & Kashmir, India, Probe (1994): (XXXIII), 4, 323.
    11. Further studies on the protective effect of Liv.52 against CD-toxicity in mammalian system (pdf)
      Rathore, H.S. and Nandi, K.K., School of Studies in Zoology, Vikram University, Ujjain, Madhya Pradesh, Indian Drugs (1992): (29), 4, 149.
    12. Effects of carbon tetrachloride and Liv.52 on the clearance rate of 131I-Rose Bengal in rat liver (pdf)
      Dhawan, D., Goel, A., Department of Biophysics, Punjab University, Chandigarh, Haryana,and Karkara, K., Department of Nuclear Medicine, Postgraduate Institute of Medical Education and Research, Chandigarh, Haryana, AMPI Medical Physics Bulletin (1991): 16, (4), 27.
    13. Treatment of mice with a herbal preparation (Liv.52) reduces the frequency of radiation-induced chromosome damage in bone marrow (pdf)
      Ganesh Chandra Jagetia and Ganapathi, N.G., Department of Radiobiology, Kasturba Medical College, Manipal, Karnataka, Mutation Research (1991): (253), 123.
    14. Preventive effects of Liv.52 on the activities of cytochrome P-450 and NADPH-dependent lipid peroxidation in the liver of carbon tetrachloride-intoxicated rats (pdf)
      Goel, A. and Dhawan, D., Department of Biophysics, Punjab University, Chandigarh, Punjab, Medical Science Research (1991): (19), 113.
    15. Influence of Liv.52 on carbon tetrachloride-induced hepatotoxicity: A biochemical study (pdf)
      Goel, A., Dhawan, D.K., Department of Biophysics, Punjab University, Chandigarh, and Gautam, C.S., Department of Pharmacology, PGIMER, Chandigarh, Punjab, Indian Journal of Pharmacology (1991): 23, 182.
    16. Role of Liv.52 in alopecia-induced by radiation and chemotherapy (pdf)
      Harbans Lal Kapoor, Rajeev K. Seam and Sanjeev Sharma, Department of Radiation and Oncology, Indira Gandhi Medical College, Shimla, Himachal Pradesh, Probe (1990): (XXIX), 3, 215.
    17. Therapeutic use of Liv.52 in beryllium-induced reproductive toxicity in rats (pdf)
      Mathur, S., Prakash, A.O. and Mathur, R. School of Studies in Zoology, Jiwaji University, Gwalior, India, Probe (1990): (XXIX), 4, 266.
    18. Recovery from beryllium-induced lesions after Liv.52 treatment (pdf)
      Prakash, A.O., Mathur, S. and Mathur, R. School of Studies in Zoology, Jiwaji Universsity, Gwalior, India, Probe (1990): (XXIX), 4, 280.
    19. Protective role of Liv.52 against histological damage due to CdCl2 toxicity in the intestine of teleost fish (pdf)
      Suresh Kothari, Bhaskar Reddy, P. and Rathore, H.S., School of Studies in Zoology, Vikram University, Ujjain, Madhya Pradesh, Probe (1990): (XXIX), 3, 220.
    20. Effects of Liv.52 against cadmium chloride-induced changes on the activity of enzyme and mucosubstances in the intestine of mystus tengara (HAM) (pdf)
      Bhasker Reddy, P. and Suresh Kothari, School of Studies in Zoology, Vikram University, Ujjain, Madhya Pradesh, Environmental Risk Assessment (1989): Dec., 188.
    21. Effect of Liv.52 on carbon tetrachloride - Induced hepatotoxicity in rabbits (pdf)
      Dhumal, M.S., Mane, I.H. and Patel, S.S., Department of Pharmacology, Rural Medical College, Loni, Shrirampur-Taluk, Ahmednagar-District, Maharashtra, Indian Journal of Pharmacology (1989): (21), 3, 96.
    22. Liv.52 protection against beryllium toxicity in female albino rats (pdf)
      Mathur, R., Mathur, S. and Prakash, A.O., School of Studies in Zoology, Jiwaji University, Gwalior, Madhya Pradesh, Reproductive Toxicology (1989): (3), 249.
    23. Liv.52 protection against cadmium-induced histomorphological changes in mice spleen, duodenum and small intestine (pdf)
      Rathore, H.S. and Hema Rawat (Miss.), School of Studies in Zoology, Vikram University, Ujjain, Madhya Pradesh, Indian Drugs (1989): (26), 10, 533.
    24. Rifampicin toxicity and Liv.52 (pdf)
      Purohit, S.D., Dilip K. Jain, Meena, R.C., Gupta, M.L., Gupta, P.R., Mathur, B.B., Gehlot, S.L. and Mehta, Y.R., Department of Respiratory Diseases and Tuberculosis, S.M.S. Medical College, Jaipur, Rajasthan, Probe (1988): (XXVII), 4, 261.
    25. Radioprotective effects of Liv.52 and tissue-reduced glutathione (GSH) in experimental rats (pdf)
      Sarkar, S.R., Singh, L.R., Uniyal, B.P. and Bhatnagar, V.S., Institute of Nuclear Medicine and Allied Sciences, Probyn Road, Delhi, The Bombay, Maharashtra Hospital Journal (1988): 4, 41.
    26. Comparative efficacy of Liv.52 and andrographis paniculata, (Nees.) in experimental liver damage in rabbits (pdf)
      Dwivedi, S.K., Sharma, M.C., Mukherjee, S.C., Jawaharlal and Pandey, N.N., Indian Veterinary Research Institute, Izatnagar, Uttar Pradesh, Indian Drugs (1987): (25), 1, 1.
    27. Effect of Liv.52 on SH-glutathione levels in carbon tetrachloride-induced liver damage (pdf)
      Kulkarni, R.D., Regional Research Institute of Unani Medicine, Grant Medical College and J.J. Group of Hospitals, Bombay, Maharashtra, Probe (1987): (XXVII), 1, 19.
    28. Beryllium-induced haematological alterations and their response to Liv.52 (pdf)
      Mathur, R., Prakash, A.O. and Mathur, S., School of Studies in Zoology, Jiwaji University, Gwalior, Madhya Pradesh, Industrial Health (1987): 25, 131.
    29. Protection of mice liver with Liv.52 against cadmium intoxication (pdf)
      Rathore, H.S. and Rita Verma, School of Studies in Zoology, Vikram University, Ujjain, Madhya Pradesh, Indian Drugs (1987): (25), 1, 11.
    30. Can Liv.52 protect mammalian kidney against toxic substances? – Results and possibilities (pdf)
      Rathore, H.S., School of Studies in Zoology, Vikram University, Ujjain, Madhya Pradesh, Indian Drugs (1987): (25), 1, 7.
    31. Effect of Liv.52 on blood sugar in beryllium nitrate-exposed rats (pdf)
      Seema Mathur, Prakash, A.O. and Mathur, R., School of Studies in Zoology, Jiwaji University, Gwalior, Madhya Pradesh, Current Science (1987): (56), 7, 322.
    32. Protective effect of Liv.52 against beryllium toxicity in rats (pdf)
      Seema Mathur, Prakash, A.O. and Mathur, R., School of Studies in Zoology, Jiwaji University, Gwalior, Madhya Pradesh, Current Science (1986): (55), 18, 899.
    33. In vitro effect of an ayurvedic liver remedy on hepatic enzymes in carbon tetrachloride treated rats (pdf)
      Piyush Bardhan, Sharma, S.K. and Garg, N.K., Central Drug Research Institute, Lucknow, Uttar Pradesh, Indian Journal of Medical Research (1985): (82), Oct., 359.
    34. Liv.52 protection against radiation-induced lesions in mammalian liver (pdf)
      Saini, M.R., Department of Zoology, University of Rajasthan, Jaipur, Rajasthan, and Saini, N., E.S.I. Hospital, Jaipur, Rajasthan, Radiobiology and Radiotherapy (1985): 26, 3, 379.
    35. Late effect of whole-body irradiation on the peripheral blood of mice and its modification by Liv.52 (pdf)
      Saini, M.R., Kumar, S., Uma Devi, P. and Saini, N., Department of Zoology, University of Rajasthan, Jaipur and Department of Paediatrics, E.S.I. Hospital, Jaipur, Rajasthan, Radiobiology and Radiotherapy (1985): (26), 4, 487.
    36. Survival of mice protected from lethal radiation by Liv.52 (pdf)
      Saini, M.R., Kumar, S., Department of Zoology, University of Rajasthan, Jaipur, Rajasthan, and Saini, N., Department of Paediatrics, E.S.I. Hospital, Jaipur, Rajasthan, Probe (1984): (XXIII), 4, 209.
    37. Liv.52 protection against late effect of radiation on mammalian spleen (pdf)
      Saini, M.R., Kumar, S., Jagetia, G.C., Department of Zoology, University of Rajasthan, Jaipur and Saini, N., Department of Paediatrics, E.S.I. Hospital, Jaipur, Rajasthan, Indian Drugs (1984): 9, 374.
    38. Effectiveness of Liv.52 against radiation sickness and dermatitis (pdf)
      Saini, M.R., Sunil Kumar, Department of Zoology, University of Rajasthan, Jaipur, Rajasthan, Jagetia, G.C., Department of Radiotherapy and Oncology, Kasturba Medical College Hospital, Manipal, Karnataka, and Navita Saini, Department of Paediatrics, E.S.I. Hospital, Jaipur, Rajasthan The Indian Practitioner (1984): December, 1133.
    39. Liver protection by Liv.52 in lipid peroxidation (pdf)
      Soman, R.N., Bhatia General Hospital, Tardeo, Bombay, Maharashtra, Probe (1984): (XXIII), 2, 110.
    40. Effect of Liv.52 on carbon tetrachloride-induced changes in hepatic microsomal drug-metabolising enzymes of the rat (pdf)
      Ira Thabrew, M., Godwin O. Emerole, Department of Biochemistry, and Subbarao, V.V., Department of Physiology, College of Medicine, University of Ibadan, Ibadan, Nigeria, Toxicology Letters (1982): 14, 183.
    41. Effect of Liv.52 on membrane lipids in carbon tetrachloride-induced hepatotoxicity in rats (pdf)
      Alok Saxena, and Garg, N.K., Biochemistry Division, Central Drug Research Institute, Lucknow, Uttar Pradesh, Indian Journal of Experimental Biology (1981): (19), 859.
    42. Clinical evaluation of Liv.52 as an adjuvant in cancer cases getting large field irradiation with or without chemotherapy (pdf)
      Krishnan Nair, M. and Chandrasekharan Nair, T., Department of Radiology and Cancer Institute, Medical College Hospital, Trivandrum, Kerala, Probe (1981): (XX), 4, 288.
    43. A case of radiation and drug-induced alopecia and premature greying cured with Liv.52 (pdf)
      Kamlakar Tripathi, Department of Medicine, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, Capsule (1979): 6, 122.
    44. Effect of Liv.52 and carbon tetrachloride on the liver protein and nucleic acids (pdf)
      Subbarao, V.V. and Gupta, M.L., Upgraded Department of Physiology, S.M.S. Medical College, Jaipur, Rajasthan, IRCS Medical Science (1979): 7, 499.
    45. Ultrastructural study on the regeneration of liver under the influence of Liv.52 (pdf)
      Prasad, G.C. and Gupta, R.C., Department of Shalya Shalakya, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, Capsule (1978): 7, 146.
    46. An experimental evaluation of protective effects of some indigenous drugs on carbon tetrachloride-induced hepatotoxicity in mice and rats (pdf)
      Singh, N. (Mrs.), Nath, R., Singh, D.R., Gupta, M.L. and Kohli, R.P., Department of Pharmacology and Therapeutics, K.G. Medical College, Lucknow, Uttar Pradesh, Quarterly Journal of Crude Drug Research (1978): (16), 1, 8.
    47. Effect of carbon tetrachloride and Liv.52 on liver microsomal protein, total protein and nucleic acids (pdf)
      Subbarao, V.V. and Gupta, M.L., Upgraded Department of Physiology, S.M.S. Medical College, Jaipur, Rajasthan, The Indian Practitioner (1978): 11, 831.
    48. Report on the combination of a liver-stimulating preparation, Liv.52 with endoxan in the treatment of cancer (pdf)
      Vaidya, M.D., Katra Hospital, Mandla, Madhya Pradesh, Probe (1978): (XVII), 2, 159.
    49. Changes in serum transaminases due to hepatotoxicity and the role of an indigenous hepatotonic Liv.52 (pdf)
      Subbarao, V.V., University of Tripoli, Tripoli, Libya, and Gupta, M.L., Upgraded Department of Physiology, S.M.S. Medical College, Jaipur, Rajasthan, Yugoslavia Physiologica Pharmacologica Acta (1976): 12.
    50. Clinical trial with Liv.52 in cases of malignant diseases treated at the barnard Institute of radiology (pdf)
      Gajaraj, A. and Munuswamy, G., Barnard Institute of Radiology, Government General Hospital, Madras, Tamil Nadu, The Antiseptic (1972): (69), 8, 570.
    51. Effect of an indigenous drug on ICG (Indocyanine Green): Clearance and autoradiographic patterns in albino rats with experimentally induced hepatotoxicity (pdf)
      Joglekar, G.V., Department of Pharmacology, B.J. Medical, Poona, Maharashtra and Leevy, C.M., Division of Liver and Nutrition, New Jersey College of Medicine and Dentistry, N.J. 07018, U.S.A., Journal of Indian Medical Profession (1970): 12, 7480.
    52. The protective action of Liv.52 against the hepatotoxicity of tetracycline in rats (pdf)
      Anonymous, Department of Pharmacology, The Himalaya Drug Co., Bombay, Maharashtra, Probe (1967): (VI), 4, 169.
    53. Allyl alcohol-induced hepatotoxicity in rats and its protection by Liv.52 (pdf)
      Joglekar, G.V. and Balwani, J.H., Department of Pharmacology, B.J. Medical College, Poona, Maharashtra Journal of Experimental Medical Science (1967): 11, 7.
    54. Effect of Liv.52 on biochemical and functional abnormalities of the liver (pdf)
      Qazi, I.H., Department of Pharmacology, The Himalaya Drug Co., Bombay, Maharashtra, Probe (1965): (V), 1, 1.
    55. Protection by indigenous drugs against hepatotoxic effects of carbon tetrachloride in mice (pdf)
      Joglekar, G.V., Chitale, G.K. and Balwani, J.H., Departments of Pharmacology and Pathology, B.J. Medical College, Poona, Maharashtra, Acta Pharmacologica et Toxicologica (1963): 20, 73.
    56. Protection by Indigenous drugs against hepatotoxic effects of carbon tetrachloride – A long term study (pdf)
      Karandikar, S.M., Joglekar, G.V., Chitale, G.K. and Balwani, J.H. Department of Pharmacology and Pathology, B.J. Medical College, Poona, India, Acta Pharmacologica et Toxicologica (1963): 20, 274-280.
    57. Effect of mercuric chloride on the survival, food-intake, body weight, histological and haematological changes in mice and their prevention with Liv.52 (pdf)</SPAN>
      Rathore, H.S. and Varghese, J., School of Studies in Zoology, Vikram University, Ujjain, Madhya Pradesh, Indian Journal of Occupational Health (Undated).
    58. Effect of a multiherbal drug on the distribution and excretion of mercury in mice treated with mercuric chloride (pdf)
      Rathore, H.S. and Varghese, J., School of Studies in Zoology, Vikram University, Ujjain, Madhya Pradesh, Indian Drugs (Undated): (32), 6, 262.
    As an adjuvant with hepatotoxic drugs

    1. Effect of spirulina and Liv.52 on cadmium Indiuced toxicity in albino rats (pdf)
      K Jeyaprakash & P Chinnaswamy Department of Biochemistry, Dr.N.G.P.Arts & Science College, Kovai Medical Center Research & Educational Trust, Coimbatore 641 014, India.
      (pdf)
    2. Effect of hepatoprotective agent Liv.52 on nutrition parameters in hemodialysis patients (pdf)
      Gordana Perunicic-Pekovic, Ljiljana Komadina, Steva Pljesa, Zorica Rasic-Milutinovic, Rodoljub Markovic, Department of Nephrology, University Hospital, Zemun-Belgrade and Natasa Milic, Institute of Statistics, Belgrade Medical School, Zemun-Belgrade, Medicine Update - Anniversary Issue, 2003, pp. 52-56.
    3. Protective effect of Liv.52 on Na+-K+-ATPase activity in paracetamol-induced hepatotoxicity (pdf)
      Kala Suhas Kulkarni*, Md. Rafiq, Gopumadhavan, S., Venkataranganna, M.V., Madhumathi, B.G. and Mitra, S.K. R&D Center, The Himalaya Drug Company, Makali, Bangalore, India, Medicine Update (2002): (10), 5, 53-56.
    4. Therapeutic efficacy of Liv.52 in paracetamol induced hepatopathy in rabbits (pdf)
      Anup Bhaumik and Sharma, M.C. Division of Experimental Medicine and Surgery, Indian Veterinary Research Institute, Izatnagar, Uttar Pradesh, India, Indian Journal Veterinary Research (2002): (11), 1, 8-17.
    5. Hepatoprotective effect of Liv.52 on antitubercular drug-induced hepatotoxicity in rats (pdf)
      Vijaya Padma, V, Suja, V. and Shyamala Devi, C.S. Department of Biochemistry, University of Madras, Guindy Campus, Madras, India. and Prema, Head-Department of Biochemistry, Tuberculosis Research Centre, Chetpet, Chennai, India, Fitoterapia (1998): (LXIX), 6, 520.
    6. Effect of phytotherapy on prevention and elimination of hepatotoxic reactions in patients with pulmonary tuberculosis and carriers of hepatitis B virus markers (pdf)
      Galitsky, L.A., Barnaulov, O.D., Zaretskii, B.V., Malkov, M.I., Konenkov, S.I., Gol’m, N.P., Tomakov, V.S., Ogarkov, P.I. and Batskov, S.S. Military Academy of Medicine, Human Brain Institute of the Russian Academy of Sciences, Saint-Petersburg, Russia, Problems of Tuberculosis, (1997): 4, 35.
    7. Hepatoprotective role of Liv.52 against hepatitis-induced by antitubercular drugs (pdf)
      Ashish Khare, Department of Medicine, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, Probe (1992): (XXXI), 3, 260.
    8. Efficacy of Liv.52 and Geriforte as adjuvant in various carcinomas (pdf)
      Durgesh Kumar Acharya, Regional Centre for Cancer Research and Treatment, Cuttack, Orissa, Probe (1986): (XXV), 3, 249.
    9. Role of Liv.52 in cyclophosphamide-induced alopecia (pdf)
      Harbans Lal Kapoor, Seam, R.K. and Sanjiv Sharma, Department of Radiation Therapy and Oncology, Indira Gandhi Medical College, Simla, Himachal Pradesh, Probe (1986): (XXV), 4, 344.
    10. Hepatoprotective role of indigenous drug Liv.52 in lepromatous leprosy (pdf)
      Pranesh Nigam and Mukhija, R.D., B.R.D. Medical College, Gorakhpur, Dayal, S.G., Government Medical College, Jammu-Tawi, Goyal, B.M. and Joshi, L.D., M.L.B. Medical College, Jhansi, Madhya Pradesh, Hansenlogia Internationalis, Brazil (1982): 7, 1, 36.
    11. Experience with Liv.52 as an adjuvant to anti-tubercular treatment (pdf)
      Vinod Kumar Gupta, The Sincere Dispensary and Nursing Home, Rori Bazar, Sirsa, Haryana, Capsule (1980): 6, 122.
    12. Effect of Liv.52 on hepatic enzymes (pdf)
      Alok Saxena and Garg, N.K., Division of Biochemistry, Central Drug Research Institute, Lucknow, Uttar Pradesh, Indian Journal of Experimental Biology (1979): 7, 662.
    13. The effect of Liv.52 on liver functions of tubercular patients receiving second line anti-tubercular drugs (pdf)
      Brij Kishore, Hazra, D.U., Sachan, A.S., Agrawal, B.M., Bharadwaj, Ashok Kumar and Mehrotra, M.M.N., Postgraduate Department of Medicine, S.N. Medical College, Agra, Uttar Pradesh, Probe (1978): (XVII), 2, 125.
    14. Some observations with Liv.52 therapy in cases of malignancy (pdf)
      Harish Kulkarni, R.S.T. Cancer Centre, Nagpur, Maharashtra, Probe (1978): (XVII), 3, 233.
    15. Effect of an indigenous (herbal) drug Liv.52 on the hepatic damage caused by oral contraceptives – A biochemical (enzymatic) approach (pdf)
      Khuteta, K.P., Upgraded Department of Physiology and Biochemistry, S.M.S. Medical College, Jaipur, Rajasthan, Probe (1978): (XVII), 2, 115.
    16. Leprous hepatitis: Clinico-pathological study and therapeutic efficacy of Liv.52 (pdf)
      Pranesh Nigam, Dayal, S.G., Goyal, B.M., Nimkhedakar, K., Joshi, L.D. and Samuel K.C., M.L.B. Medical College, Jhansi, Uttar Pradesh, Leprosy in India (1978): (50), 2, 185.
    17. Tissue culture and electron microscopic study on regeneration of liver with Liv.52 (pdf)
      Prasad, G.C., Department of Shalya and Surgical Research Laboratory, Institute of Medical Science, Banaras Hindu University, Varanasi, Uttar Pradesh,Capsule (1978): 6, 122.
    18. Liv.52-induced modification of barbiturate hypnosis in albino rats (pdf)
      Joglekar, G.V., Saraf, A.P., Moholkar, A.L. and Shirole, M.V. (Miss.), Department of Pharmacology, B.J. Medical College, Pune, Maharashtra, Maharashtra Medical Journal (1977): (XXIV), 2, 67.
    19. Paracetamol-induced hepatotoxicity and the protective effect of Liv.52 (pdf)
      Mujumdar, S.M. and Kulkarni, R.D., Department of Pharmacology, B.J. Medical College, Pune, Maharashtra, The Indian Practitioner (1977): (XXX), November, 479.
    20. Anorexia in osteoarticular tuberculosis (pdf)
      Dabral, P.K., Srivastava, M.K. and Madhu Dabral (Mrs.), M.L.B. Medical College, Jhansi, Madhya Pradesh, Probe (1976): (XV), 3, 199.
    21. Electron microscopic study on the effect of Liv.52 on carbon tetrachloride treated liver (pdf)
      Prasad, G.C., Department Shalya and Surgical Research Laboratory, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, Journal of Research in Indian Medicine, Yoga and Homeopathy (1976): 4, 38.
    22. Role of Liv.52 in hepatomegaly associated with childhood tuberculosis (A clinico-histopathological study) (pdf)
      Kumar, P. and Shishupal Ram, Department of Paediatrics, Patna Medical College Hospital, Patna, Bihar, The Indian Practitioner (1975): 10, 535.
    23. Place of Liv.52 as an adjuvant to chemotherapy of malignant diseases (pdf)
      Munuswamy, G. and Gajraj, A., Barnard Institute of Radiology and Cancer, Government General Hospital and Madras Medical College, Madras, Tamil Nadu, Probe (1975): (XV), 1, 1.
    24. Effect of Liv.52 on the liver in vitro (pdf)
      Prasad, G.C., Department of Shalya and Surgical Research Laboratory, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, Journal of Research in Indian Medicine (1975): 4, 15.
    25. Effect of Liv.52 on regeneration of liver cells in tissue culture – A preliminary report (pdf)
      Prasad, G.C., Department of Shalya Shalakya and Surgical Research Laboratory, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, Journal of Research in Indian Medicine (1974): (9), 2, 60.
    26. Liv.52 as adjuvant therapy with hepatotoxic and cytotoxic drugs (pdf)
      Vaidya, M.D., Katra Hospital, Mandla, Madhya Pradesh, Probe (1974): (XIII), 2, 73.
    27. Liv.52 improves thioacetazone tolerance (pdf)
      Major Jayaram, C.N., T.B. Sanatorium, Austinpatti, Madurai, Tamil Nadu, Probe (1969): (VIII), 4, 160.
    Miscellaneous

    1. Effect of Liv.52 in digestive disorders among children (pdf)
      Khrushcheva, N.A. and Safronova, L.E., State Medical Academy based in Ural, Regional Children's Clinical Hospital, Ekaterinburg, Russia, Capsule (2002): (XLI), 4, January / March.
    2. Use of hepatoprotective agents in hepatomegaly syndrome in children: An experience with Liv.52 Syrup (pdf)
      Otilia Marginean, MD, PhD, Ioana Micle, MD, PhD, Maria Lesovici, MD, PhD, Pediatric Hospital "Louis Turcanu", Timisoara, Romania, Raluca Balean, MD, Budiu Ioana, MD, County Hospital Nr. 1, Timisoara, Romania, and Edited by: Kala Suhas Kulkarni, MD, MCPS Medical Advisor, R&D Center, The Himalaya Drug Company, Bangalore, Karnataka, India, Medicine Update (2002): (10), 8, 57.
    3. Physiological Icterus of the newborn and the role of Liv.52 (pdf)
      Goel, S.P., Lecturer, Department of Pediatrics, Garg, B.K., Professor and Head of the Department of Pediatrics Sharma, D.K., Professor in the Department of Pediatrics, Upadhyay, V.K., Lecturer in the Department of Pediatrics, L.L.R.M. Medical College, Meerut, India, Probe (1994): (XXXIV), 1, 45.
    4. Prevention of mercuric chloride-induced histopathological changes in the small intestine of mice with Liv.52 (pdf)
      Johnson, V. and Rathore, H.S., Cell Biology Unit, School of Studies in Zoology, Vikram University, Ujjain, Madhya Pradesh, Indian Journal of Medical Sciences (1994): (48), 11, 253.
    5. Chemopreventive action of Liv.52 on DMBA-induced papillomagenesis in skin of mice (pdf)
      Ritu Prashar and Ashok Kumar, Department of Zoology, University of Rajasthan, Jaipur, Rajasthan, Indian Journal of Experimental Biology (1994): (32), Sep., 643.
    6. Evaluation of the role of Liv.52 treatment in swiss albino mice during pre- and post-natal development (pdf)
      Saini, M.R., Sharma, K. and Kumar, A., Radiation Biology Laboratory, University of Rajasthan, Jaipur, India, Probe (1994): (XXXIII), 4, 343.
    7. Cytogenetic effects of Liv.52 on the male germline cells of poekilocerus pictus (Acrididae: Orthoptera) (pdf)
      Edward Gururaj, M. and Uma, O., Department of Studies in Zoology, University of Mysore, Mysore, Karnataka, Journal of Mysore University (1993): (33), 181.
    8. Role of Liv.52 and Geriforte as general metabolic tonics in drug addicts (pdf)
      Jain, N.C., Government Rajindera Medical College and Hospital, Patiala, Singal, R.P., Dayanand Hospital, Ludhiana, Punjab, and Shahi, S.R., S.S.M.D. Ayurvedic College and Hospital, Moga, Punjab, Probe (1992): (XXXII), 1, 32.
    9. Absence of teratogenic effect of Liv.52 in albino rats (pdf)
      Singh, N., Verma, P. and Mishra, N., Upgraded Department of Pharmacology and Therapeutics, K.G. Medical College, Lucknow, Uttar Pradesh, Journal of Biological and Chemical Research (1990): (9), 445.
    10. Inhibition of clastogenic effect of radiation by Liv.52 in the bone marrow of mice (pdf)
      Ganesh Chandra Jagetia and Ganapathi, N.G., Department of Radiobiology, Kasturba Medical College, Manipal, Karnataka, Mutation Research (1989): (224), 4, 507.
    11. Lack of teratogenicity of Liv.52 (pdf)
      Chauhan, B.L., Gurjar, P.A. and Kulkarni, R.D., R&D Centre, The Himalaya Drug Co., Bombay, Maharashtra, Probe (1988): (XXVIII), 1, 36.
    12. Liv.52 protection against radiation-induced abnormalities on mammalian prenatal development (pdf)
      Saini, M.R., Kumar, S., Department of Zoology, University of Rajasthan, Jaipur, Rajasthan, and Saini, N., Department of Paediatrics, E.S.I. Hospital, Jaipur, Rajasthan, Radiobiology and Radiotherapy (1985): (26), 3, 385.
    13. The treatment of non-suppurative hepatic amoebiasis with Liv.52 as an adjuvant to antiamoebic drugs (pdf)
      Bose, S.L. and Rout, A.K., Department of Medicine, S.C.B. Medical College, Cuttack, Orissa, Indian Medical Journal (1983): 1, 3.
    14. Role of Liv.52 in the treatment of pityriasis alba (pdf)
      Chakraborty, A.K., G.T. Road, Kalitala, Serampore, West Bengal, Capsule (1983): 1, 9.
    15. Liv.52 in burns cases (pdf)
      Malla, C.N. and Surinder Singh, Medical College and H.M.H.S. Hospital, Srinagar, Jammu and Kashmir, Probe (1982): (XXII), 1, 24.
    16. Clinical trial of Liv.52 in burns (pdf)
      Parangusa Das, R.A., Vijayalakshmi, B. and Subhashini, M.,Victoria Hospital, Bangalore, Karnataka, Probe (1982): (XXI), 3, 192.
    17. Role of Liv.52 in psychiatric illness (pdf)
      Rustom N. Burjorjee, Calcutta Medical Centre, London Street, Calcutta, West Bengal, Capsule (1982): 5, 98.
    18. A case study on Liv.52 an adjuvant in diabetes mellitus (pdf)
      Sinha, A.K., P.T.P.S. Hospital, Patralu, District, Hazaribagh, Bihar, Capsule (1982): 8, 178.
    19. Effect of Liv.52 on liver lipids (pdf)
      Alok Saxena, Sharma, S.K. and Garg, N.K., Department of Biochemistry, Central Drug Research Institute, Lucknow, Uttar Pradesh, Indian Journal of Experimental Biology (1980): 11, 1330.
    20. Potentiation of barbiturate hypnosis in rats by Liv.52 (pdf)
      Dhume, V.G., Goa Medical College, Panaji, Goa, and Bijlani, C.J., T.N. Medical College, Bombay, Maharashtra, The Clinician (1979): (43), 2, 59.
    21. Evaluation of Liv.52 in the treatment of jaundice with pregnancy (pdf)
      Arun Kumar Mitra and Abhik De, Calcutta Medical College, West Bengal, Probe (1978): (XVII), 2, 143.
    22. Liv.52 in herpes-progenitalis (pdf)
      Iswar Tanwani, Howrah Road, Deolali Cantonment, Nasik District, Maharashtra, Journal of National Integrated Medical Association (1976): (18), 3, 98.
    23. Effect of Liv.52 on serum lipids in normal and patients suffering from ischaemic heart disease (pdf)
      Rao, C.R. and Subba Rao, A., Bowring and Lady Curzon Hospital, Postgraduate and Research Institute, Bangalore, Karnataka, Probe (1975): (XIV), 3, 177.
    24. Radioactive Rose Bengal test of liver function – A preliminary report of Liv.52 trial (pdf)
      Rajagopal, K.R., Radio-Isotope Department, Barnard Institute of Radiology, Government General Hospital, Madras, Tamil Nadu, Probe (1974): (XIV), 1, 50.
    25. A clinical study of the therapeutic efficacy of Liv.52 as an adjuvant in the treatment of hepatic amoebiasis (pdf)
      Sethi, J.P. and Suresh Meratwal, Department of Medicine, S.M.S. Medical College and Attached Hospital, Jaipur, Rajasthan, Probe (1973): (XII), 3, 129.
    26. Gastrointestinal allergy treated with Liv.52 – A case report (pdf)
      Tripathi, A.R., Department of Forensic Medicine, Institute of Medical Services, Banaras Hindu University, Varanasi, Uttar Pradesh, Capsule (1973): June/July, 30.
    27. Liv.52 in dermatology (pdf)
      Behl, P.N., Skin Institute, Delhi, Probe (1972): (XI), 2, 100.
    28. Therapy of toxaemias of pregnancy (pdf)
      Narone, J.N., and Raj Narone (Mrs.), Department of Gynaecology and Obstetrics, Patna Medical College, Patna, Bihar, Probe (1972): (XI), 2, 120.
    29. Some studies on physiological jaundice of the new-born (pdf)
      Srivastava, J.R., Bhalla, J.N. and Arora, A., G.S.V.M. Medical College, Kanpur, Uttar Pradesh, Probe (1972): (XII), 1, 4.
    30. Liv.52 in vitiligo (pdf)
      Punshi, S.K. Consultant Dermatologist and Abroal, S.K., Amravati, M.S., Probe (1970): (X), 1, 12.
    31. Studies with Liv.52 (pdf)
      Lala Surajnandan Prasad, Department of Paediatrics, Patna University, Patna, Bihar and Devendra Tripathy, Hospital for Children, Patna Medical College Hospital, Patna, Bihar, Probe (1969): (IX), 1, 1.
    32. Metabolic effect of an indigenous compound on sportsmen (pdf)
      Mathur, D.N., The National Institute of Sports, Patiala, Punjab, Probe (1969): (VIII), 4, 144.
    33. Liv.52 in general practice (pdf)
      Shah, N.B., Malegaon City, Nasik, Maharashtra, Probe (1969): (VIII), 3, 101.
    34. A clinical study – Physiological jaundice in neonates (pdf)
      Chafekar, V.D., Annapoornabai Maternity and Nursing Home, Gadag, Karnataka, Probe (1968): (VII), 3, 85.
    35. Observations on Liv.52 (pdf)
      Patrao, S., B.Y.L. Nair Hospital and T.N. Medical College, Bombay, Maharashtra, Journal of Indian Medical Profession (1957): 8, 1878.
    36. Ascitis due to liver deficiency treated with an indigenous drug (pdf)
      Sule, C.R., Sathe, P.M., Koshy, M.C. and Desphande, M.S., The Indian Practitioner (1956): (IX), 4, 357.
    "The only way you can hurt the body is not use it. Inactivity is the killer and, remember, it's never too late."
    ~Jack Lalanne



Posting Permissions

  • You may not post new threads
  • You may not post replies
  • You may not post attachments
  • You may not edit your posts
  •