Protective effects of vitamin E on experimentally induced hepatotoxicity in rats

D-galactosamine (D-GalN) and lipopolysaccharide (LPS) administration lead to increase production of reactive oxygen species (ROS). Increased oxidative stress caused injury of liver cells and therefore increased leakage of liver cell enzymes as alanine transaminase (ALT) and aspartate transaminase (AST) into the systemic circulation. Increased ROS productions also, lead to decreased non-enzymatic antioxidant such as glutathione (GSH). Vitamin E used in this study as it is a powerful antioxidants.This study was designed to elucidate the protective effectofvitamin E on D-GalN/LPS induced hepatotoxicity in albino Wister rats. Acute hepatic failureinduced by intraperitoneal injection of 500 mg/kg D-GalN and 50 µg/kg LPS body weight of adult albino rats.Vitamin E was used as prophylaxis in doses of 400 mg/Kg body weight. Serum ALT and AST were measured by kinetic method. Liver GSH was measured by using colorimetric kits. It can be concluded that administration of D-GalN/LPS caused rat liver injury that was through excess ROS generation. Vitamin E succeeded in ameliorating the deleterious effects of D-GalN/LPS induced oxidative stress.