Objective To investigate the protective effect of zinc in CCl4-induced hepatotoxicity. Methods Rats were treated with zinc acetate for four days. The zinc doses were 5 mg Zn/kg and 10 mg Zn/kg body weight respectively. Two groups of the zinc acetate-treated rats were later challenged with a single dose of CCl4 (1.5 mL/kg body weight). Results Compared to control animals, the plasma of rats treated with CCl4 showed hyperbilirubinaemia, hypoglycaemia, hypercreatinaemia and hypoproteinaemia. When the animals were however supplemented with zinc in form of zinc acetate before being dosed with CCl4, the 5 mg Zn/kg body weight of zinc acetate reversed the hypoproteinaemia induced by CCl4, whereas the 10mg Zn/kg body weight of zinc acetate reversed the hypoglycaemia, hyperbilirubinaemia and hypercreatinaemia induced by CCl4. Conclusion The 10mg Zn/kg body weight of zinc acetate is more consistent in protecting against CCl4 hepatotoxicity. The possible mechanisms of protection are highlighted. Objective To investigate the protective effect of zinc in CCl4-induced hepatotoxicity. Methods Rats were treated with zinc acetate for four days. The zinc doses were 5 mg Zn / kg and 10 mg Zn / kg body weight respectively. Two groups of the zinc acetate Results Compared to control animals, the plasma of rats treated with CCl4 showed hyperbilirubinaemia, hypoglycaemia, hypercreatinaemia and hypoproteinaemia. When the animals were yet supplemented with the zinc in form of zinc acetate before being dosed with CCl4, the 5 mg Zn / kg body weight of zinc induced by the hypoproteinemia induced by CCl4, but the 10 mg Zn / kg body weight of zinc induced by the hyperchronicirubricaemia, hyperbilirububinaemia and hypercreatinaemia by CCl4. Conclusion The 10 mg Zn / kg body weight of zinc acetate is more consistent in protecting against CCl4 hepatotoxicity. The possible mechanisms of protection are highligh ted.