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Here's a study on Liv-52 for liver protection.

Indian J. Pharmac. (1989) 21 : 96-93 INDIAN JOURNAL OF PHARMACOLOGY
Department of Pharmacology,
Rural Medical College,
Loni, Taluka - Shrirampur, Dist. Ahmednagar

I. Carbon Tetrachloride was administered to induce hepatotoxocity in male rabbits. Serum enzymes ACT and AST were monitored. In one group of Carbon Tetrachloride treated rabbits, Liv. 52 was administered orally by Ryle’s tube. Observations were made for five days. Liv. 52 produced marked reduction in ALT levels whereas the effect of Liv. 52 on AST levels were less marked. Reasons for this differential effect of Liv. 52 on ALT and AST levels are discussed.
Key phrases : Hepatotoxicity, Serum enzyme, Rabbit, Carbon-tetrachloride.

Viral hepatitis and alcoholic liver disease continue to be major health problems. Though good hygiene can help limit the spread of the first and abstinance from alcohol can prevent the second, both these are unlikely to be achieved in the near future. Modern medicine offers little by way of cure. Several indigenous herbs are reputed to be useful in viral hepatitis. Their clinical evaluation is difficult because of variable and self-limiting nature of the disease. The experimental evaluation is mostly done in rats by studying of the protective effect against carbon tetrachloride induced damage. The response of the rats to carbon tetrachloride is known to be variable and specificity of enzyme change: is doubtful. Therefore, it is necessary to develop more reliable method for testing hepatoprotective agents. Hence it was decided to use rabbits as test animals. Liv. 52 is widely used as hepatoprotective agent and therefore it was decided to test the protective effect, if any, of Liv. 52.

12 male rabbits weighing between 1.3 kg and 2.5 kg were used in this study. Rabbits were housed individually and were fed on natural rabbit feeds. The rabbits were divided into two groups. Group I acted as control and Group II acted as test group for protective effect of Liv. 52. Blood was collected from ear vein to estimate Alanineamino transferase (ALT-formerly SGPT) and Aspertate-amino transferase (ASTformerly SGOT). Thereafter each rabbit received carbon tetrachloride in the dose of 0.5 ml/kg intraperitoneally as a single dose. Rabbits in Group I received water once daily orally for 5 days and rabbits from Group II received Liv. 52 syrup in the dose 5.0 ml/kg per day orally for 5 days, Dose of Liv. 52 was calculated by extrapolating human adult dose according to the surface area ratio (1). Blood samples were collected from ear vein every 12 hours on the first two days and every 24 hours on the following 3 days for serum ALT and AST estimations. The enzyme activities were determined by the method of Reitmann and Frankel(4).

The fasting serum enzyme levels were within the normal range for all rabbits prior to carbon tetrachloride administration (5). After carbon tetrachloride administration in the control group ALT levels doubled in 12 hours and were progressively rising up to 96 hours. On the other hand AST levels doubled in 12 hours, reached a peak at 48 hours, but started declining at 72 hours. In the Liv. 52 treated group ALT levels doubled in 12 hours but started declining at 24 hours, and reached normal levels at 96 hours. The levels of AST in Liv. 52 treated group increased at 12 hours but decreased at 24 hours, rose again to reach a peak at 48 hours and decreased after 72 hours.

The results of this study are interesting in that the response of ALT and AST to carbon tetrachloride are different. ALT shows a much larger increase and progressive rise. AST shows much smaller increase with peak after 48 hours and then decline. It is known that ALT concentrations are high in the liver and very low in the other tissues (3). AST on the other hand is found in high concentrations in the heart, skeletal muscle and kidney apart from the liver (3). Carbon tetrachloride is known to damage other tissues also. Therefore ALT levels give a reliable guide to liver cell damage whereas AST levels are not indicative of liver damage. It is more specific for cardiac necrosis and these effects are seen after 48 hours. In the present study AST levels rose in 12 hours, reached peak at 48 hours and fell slowly at 72 hours. The effect of Liv. 52 is also remarkable in that ALT levels were reduced from 24 hours onwards and reached normal at 96 hours. The AST levels rose at a 12 hours but fell at 24 hours and rose again at 48 hours. This probably indicates that the rise in AST in the first 24 hours is due to liver damage and delayed rise reaching a peak at 48 hours is due to damage to other tissues. Therefore, the first peak at 24 hours is suppressed by Liv. 52, but it has no effect on the second peak. The method employing rabbits therefore appears superior in studying hepatotoxic agents and Liv. 52 showed hepatoprotective action in this study.

M. N. GHOSH (1971) : Toxicity studies. Fundamentals of experimental Pharmacology; pp. 85: Published by Scientific Book Agencies, 22, Raja Woodmint Street, Calcutta.

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HAROLD VARLEY (1969) : Enzymes; Practical Clinical Biochemistry, Fourth Edition; Published by Gulab Vazirani for Arnold Heinemann Publishers (India) Pvt. Ltd; pp 296; AB/9 Safdarjang Enclave, New Delhi.

HAROLD VARLEY, ALAN H. GOWENLOCK, MAURICE BELL (1980) : Enzymes; Practical Clinical Biochemistry : Vol I, Fifth Edition; p. p. 741-742; William Heinewann Medical Books Ltd; London. Clinical Biochemistry Reference Values (1983) : A Manual of Laboratory Techniques. Published by : National Institute of Nutrition; p. p. 276; ICMR. Hyderabad.