Zinc deficiency enhances sensitivity to carbon tetrachloride-induced hepatotoxicity in rats.

Abstract Zinc (Zn) is an essential nutrient that is required in humans and animals for many physiological functions, including immune and antioxidant functions, growth and reproduction. The present study was conducted to examine the influence of Zn deficiency on the protective action against mild oxidative stress induced by a low dose of carbon tetrachloride (CCl 4 ) in rats. Male Wistar rats were administered 125 or 250 μL/kg body weight CCl 4 , which caused mild or no elevation of serum LDH, AST and ALT enzyme levels in rats fed a diet with adequate Zn. Treatment with CCl 4 (125 μL/kg) caused a significant release of these enzymes into the serum of rats fed a Zn-deficient diet but not in those given a diet with adequate Zn. Furthermore, no histological abnormalities were observed in CCl 4 -untreated rats fed either a diet with adequate Zn or a Zn-deficient diet or in CCl 4 (125 μL/kg)-treated rats fed a diet with adequate Zn. In CCl 4 (125 μL/kg)-treated rats fed a Zn-deficient diet, however, we observed associated collagen accumulation in the liver and hepatic necrosis. The degree of fibrosis was also more severe in CCl 4 (250 μL/kg)-treated rats fed a Zn-deficient diet. These results show that zinc deficiency during an oxidative stress injury negates the protective actions of certain treatments that normally block oxidative damage. The present study suggests that Zn plays an important role in regulating the antioxidative defense system under mild CCl 4 toxic conditions.