Oa. Al-shabanah et al., Protective effect of aminoguanidine, a nitric oxide synthase inhibitor, against carbon tetrachloride induced hepatotoxicity in mice, LIFE SCI, 66(3), 2000, pp. 265-270
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.