| RESEARCH PAPER |
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| Year : 1998 | Volume
: 30
| Issue : 4 | Page : 233-238 |
Effect of Liv.100 against antitubercular drugs (isoniazid, rifampicin and pyrazinamide) induced hepatotoxicity in rats
SD Saraswathy, V Suja, Gurumurthy Prema, Devi CS Shyamala
Correspondence Address:
S D Saraswathy
 Source of Support: None, Conflict of Interest: None  | Check |
Objectives: To assess the protective effect of Liv.100 against antitubercular drugs (isoniazid (INH), rifampicin (RMP) and pyrazinamide (PZA)) induced hepatotoxicity in rats.
Methods:The simultaneous treatment of Liv.100 (400 mg/kg body weight) on antitubercular drugs (INH, RMP and PZA) induced lipid peroxidation in liver was studied in rats. Levels of marker enzymes such as lactate dehydrogenase, aspartate amino transferase, alanine amino transferase and alkaline phosphatase were assessed in liver and serum. The glutathione content and the activities of antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S- transferase were estimated in liver. The levels of lipid peroxides and the activities of Na +K+ ATPase, Ca2+ ATPase and Mg2+ ATPase were also assayed in the liver of experimental groups.
Results: In antitubercular drugs administered rats, a significant decrease was observed in the levels of marker enzymes in the liver with a corresponding increase in their levels in serum. The levels of lipid peroxidase (in terms of YBA reactants") were increased significantly in their serum and liver. The activities of Na+K+ ATPase, Ca2+ ATPase and Mg2+ ATPase were decreased significantly in their liver. The glutathione content and the activities of antioxidant enzymes decreased significantly in the liver of antitubercular drugs administered rats when compared to normal control. Simultaneous administration of Liv. 100, showed near normal levels of marker enzymes, and the levels of lipid peroxides glutathione content on comparison with normal control.
Conclusion: Simultaneous treatment with Liv. 100 offers protection against hepatotoxicity induced by antitubercular drugs by reducing lipid peroxidation and restoring the antioxidant defense system.
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