RESUMO
Oxidative damage is involved in the pathogenesis of various, hepatic injuries. In the present study the capacity of L-carnitine as an antioxidant to protect against carbon tetrachloride [CCl[4]]-induced oxidative stress and hepatotoxicity in rats was Cairo. Egypt investigated. Daily oral administration of CCl[4]100 mg/kg in corn oil for 4 weeks produced a marked significant elevation in serum, alanine aminotransferase [ALT], aspartate aminotransferase [AST], alkaline phosphatase [ALP], lactate dehydrogenase [LDH], and alpha fetoprotein [AFP]. Hepatic lipid peroxidation, quantified as malondialdehyde [MDA] was significantly increased, while the activity of the two antioxidant enzymes; glutathione peroxidase [GPx] and superoxide dismutase [SOD] in the liver were significantly reduced. Histopathological and histochemical analyses of the liver of rats treated with CCl[4] revealed centrilobular necrosis with lymphocytic infiltration between hepatocytes. The hepatocytes were damaged in the form of fatty degeneration, vacuolization, ballooning with bundles of fibrous tissue surrounding the portal tracts and dissecting the parenchyma. Concurrent administration of L-carnitine [50 mg/kg/day; s.c.] with CC!4 for 4 weeks produced a significant reduction of aminotransferases together with normalization of ALP and LDH activities as well as AFP level. The biochemical parameters of oxidative stress were improved. Hepatic MDA concentration was significantly reduced, while the activities of the hepatic antioxidant enzymes GPx and SOD were significantly increased. These effects were paralleled with an improvement of the histopathological changes induced by CCl[4], where the hepatic architecture was preserved by L-carnitine treatment. Therefore, the results of this study show that L-carnitine can be proposed to protect the liver against CCl[4]-induced oxidative damage in rats, and the hepatoprotective effect might be correlated with its antioxidant and free radical scavenger effects