Ameliorative effect of vitamin E on potassium dichromate-induced hepatotoxicity in rats

Hexavalent chromium [Cr (VI)]-mediated oxidative stress causes severe hepatic toxicity. This study aims to investigate the protective role of oral vitamin E administration against potassium dichromate (K2Cr2O7)-induced hepatotoxicity. Adult male rats (Rattus norvegicus, n=24) weighing 150–180 g were used and divided into 4 groups (n= 6 per group): the control group received distilled water; control + vitamin E group received vitamin E (100 mg/kg b.w.); Cr group received K2Cr2O7 (8 mg/kg b.w.), and Cr +vitamin E group received K2Cr2O7+ vitamin E. All treatments were administered orally on a daily basis for 6 weeks. There was a significant accumulation of Cr in the livers of the Cr group compared with the control group. In addition, exposure to K2Cr2O7 induced significant increases in the level of thiobarbituric-reactive substances (TBARS) and significant decreases in glutathione (GSH) content and superoxide dismutase (SOD) activity in the Cr group compared with the control group. Moreover, livers of the Cr group showed major histological alterations, such as severe necrosis, increased lymphocytic infiltration, and a significant decrease in the DNA content. Oral vitamin E administration concomitant with K2Cr2O7 ameliorated all these changes and resulted in normal hepatic histological and cellular contents. In conclusion, oral vitamin E administration has a hepatoprotective role against K2Cr2O7-induced hepatotoxicity in rats.