Protective effect of L-carnitine against carbon tetrachloride-induced liver injury in rats

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

Dimiethyl-4,4' -dimethoxy-5,6,5',6' dimethylenedioxybiphenyl-2,2' -dicarboxylate [DDB] reduces the burden of alcohol-induced liver toxicity

Alcohol consumption is a risk factor for hepatitis that may lead to alcoholic cirrhosis, a major cause of death in many parts of the world. DDB is a hepatoprotective drug which is mainly used for treatment of chronic persistent and active hepatitis. The aim of the present study was to evaluate the protective effects of DDB against alcohol-induced liver injury and free radical generation in rats. Fifty male rats were divided into five treatment groups and treated for 4 weeks with alcohol 7.9 g/kg b.w. and DDB 50 mg/ kg b.w. during or before alcohol administration. The results revealed that alcohol administration resulted in a significant increase in MDA, NO, IL-1 alpha, TNF- alpha, leptin, cholesterol, TG, LDL-cholesterol, ALT, procollagen III, Pi-GST, bilirubin and estradiol Whereas, it caused a significant decrease in CAT, SOD, GPX and testosterone. Treatment with DDB during or before alcohol administration resulted in a significant improvement in all the tested parameters and succeeded to restore their values towards the normal values of the control Moreover, treatment with DDB during alcohol administration was more effective than the treatment before alcohol administration.