Protective effect of aminoguanidine, a nitric oxide synthase inhibitor, against carbon tetrachloride induced hepatotoxicity in mice

The present study was undertaken to evaluate the effect of aminoguanidine ( AG) on carbon tetrachloride (CCl4)-induced hepatotoxicity. Treatment of mic e with CCl4 (20 mu l/kg, i.p.) resulted in damage to centrilobular regions of the liver, increase in serum aminotransferase and rise in lipid peroxide s level 24 hours after CCl4 administration. Pretreatment of mice with AG (5 0 mg/kg, i.p.) 30 minutes before CCl4 was found to protect mice from the CC l4-induced hepatic toxicity. This protection was evident from the significa nt reduction in serum aminotransaferase, inhibition of lipid peroxidation a nd prevention of CCl4-induced hepatic necrosis revealed by histopathology. Aminoguanidine, a relatively specific inhibitor of inducible nitric oxide s ynthase, did not inhibit the in vitro lipid peroxidation. Taken together, t hese data suggest a potential role of nitric oxide as an important mediator of CCl4-induced hepatotoxicity.