Bisphenol A (BPA), nonylphenol (NP) and octylphenol (OP) are endocrine-disrupting chemicals that has been shown to exert both toxic and estrogenic effects on mammalian cells. The aim of this study was to investigate if BPA, NP and OP induce oxidative stress on the brain tissue of male rats and if co-administration of vitamin C, an antioxidant, can prevent any possible oxidative stress. The male rats were divided into seven groups as control (vehicle), BPA, NP, OP, BPA+ C, NP + C, OP + C. BPA, OP and NP (25 mg/(kg day)) were administrated orally to male Wistar rats for 45 days. In vitamin C co-administration groups (BPA+ C, NP + C, OP + Q, vitamin C (60 mg/(kg day)) were administrated orally along with BPA, OP and NP (25 mg/(kg day)) treatments. The rats in the control group received olive oil orally. The final body and absolute organ weights of treated rats did not show any significant difference when compared with the control group. Also, there were no significant difference in relative organ weights of BPA, NPOP, BPA+ C and NP + C groups when compared with control group. Only, relative organ weights were increased significantly in OP + C group compared with control group. Decreased levels of reduced glutathione (GSH) were found in the brains of BPA, NP, OP treated rats. The end product of lipid peroxidation, malondialdehyde (MDA), appeared at significantly higher concentrations in the BPA, NP, and OP treated groups when compared to the control group. On the other hand, there were no changes in the brain MDA and GSH levels of BPA + C, NP + C and OP + C groups compared with BPA, NP and OP treatment groups, respectively. in histopathologic examination, the vitamin C co-administrated groups had much more hyperchromatic cells in the brain cortex than that observed in the groups treated with only BPA, NP, and OP. The results of this study demonstrate that BPA, NP and OP generate reactive oxygen species that caused oxidative damage in the brain of male rats. In addition, vitamin C co-administration along with BPA, NP, and OP aggravates this oxidative damage in the brain of rats. (C) 2008 Elsevier Ireland Ltd. All rights reserved.