We aimed to evaluate roles of hepatic ascorbic acid in ddY strain mice after a single injection of lead acetate (100μmol/kg body weight, i.p.). Lead decreased glutathione content, inhibited glutathione S-transferase activity, and increased calcium content in the liver four days after the injection. These lead-induced alterations were significantly antagonized by the treatment of mice with a diet containing 1(w/w) % ascorbyl stearate ester (ASE) for three days before and four days after lead injection, whereas ascorbate content was largely elevated in the livers of animals treated with both lead and ASE. Furthermore, the production of NADPH was enhanced by not only lead injection but also ASE-feeding. These results suggest that ASE-feeding could ameliorate cell damage through the restoration of intracellular redox states
