Bisphenol A, an environmental contaminant, widely used as a monomer in 
polycarbonate plastics, has been shown to cause abnormalities in liver of rats 
and mice. The nature and mechanism of action of bisphenol A on liver is not 
clear. The aim of the present study was to investigate if bisphenol A induces 
oxidative stress in the liver of rats and if co-administration of vitamin C, an 
antioxidant, can prevent oxidative stress. Bisphenol A (0.2, 2.0 and 20 micro 
g/kg body weight per day) and bisphenol A+vitamin C (0.2, 2.0, 20 micro g+40 
mg/kg body weight per day) was orally administered to rats for 30 days. After 24 
h of the last treatment, rats were killed using overdose of anesthetic ether. 
Body weights of the animals and the weights of liver showed no significant 
changes. The activities of antioxidant enzymes, superoxide dismutase, catalase, 
glutathione reductase and glutathione peroxidase were decreased in mitochondrial 
and microsome-rich fractions of liver. The levels of hydrogen peroxide and lipid 
peroxidation increased in the treated rats when compared with the corresponding 
group of control animals. Activity of alanine transaminase, a marker enzyme of 
hepatic injury remained unchanged in the treated rats as compared with the 
corresponding control rats. Co-administration of bisphenol A and vitamin C 
showed no changes in the activities of superoxide dismutase, catalase, 
glutathione reductase and glutathione peroxidase and in the levels of hydrogen 
peroxide and lipid peroxidation as compared with the corresponding control 
groups. The results indicated that bisphenol A induces oxidative stress in the 
liver of rats by decreasing the antioxidant enzymes. Co-administration of 
vitamin C reversed the effects of bisphenol A-induced oxidative stress in the 
liver of rats.