Polybrominated diphenyl ethers (PBDEs) are used as flame retardant additives. They are ubiquitous in the environment and bioaccumulate in humans and wildlife. However, little is known about their potential toxicological properties. In this study, we investigated the modifications in endogenous antioxidant capacity and oxidative damage in several brain sections and the possible behavioral effects induced by the exposure to one of the most persistent PBDE congeners, the 2, 2', 4, 4', 5-pentabromodiphenyl ether (BDE-99). Adult male rats (10/group) received BDE-99 by gavage at single dose of 0, 0.6 or 1.2 mg/kg/body weight. Forty-five days after the exposure, the following behavioral tests were conducted out: open-field activity, passive avoidance and Morris water maze. Cortex, hippocampus and cerebellum were also removed and processed to examine the following stress markers: reduced glutathione (GSH), oxidized glutathione (GSSG), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione-S-transferase (GST), superoxide dismutase (SOD), catalase (CAT) and thiobarbituric acid reactive substances (TBARS). No effects in behavioral tests were observed. Otherwise, brain endogenous antioxidant capacity was affected. Cerebellum was the most afected organ. BDE-99 exposure significantly decreased SOD, CAT and GR activities al the dose of 1.2 mg/kg/body weight. Moreover, a decrease in CAT and SOD activities was observed in cortex and hippocampus respectively. In conclusion, oxidative damage could be a mechanism for BDE-99 toxicity.