Polybrominated diphenyl ethers (PBDEs) have recently been shown to be on the increase in the environment and in human milk. The most commonly found PBDE congener in human milk is 2,2',4,4',5-penta BDE (BDE-99). The aim of the present study was to investigate the neurotoxic effects of BDE-99 (2 mg kg(-1)d(-1)) administration, from gestational day 6 to postnatal day (PND) 21, on neurobehavioural development and redox responses in offspring. Neurobehavioural development analysis revealed a delayed appearance of cliff drop and negative geotaxis reflexes in the exposed group. Furthermore, developmental exposure to BDE-99 also affected learning and memory functions during adolescence. On PND 37, the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) was reduced, while increases in hydrogen peroxide, lipid peroxidation, nitric oxide and electron spin resonance signal intensities were observed in the hippocampus of BDE-99-treated animals. However, the activity of SOD and GSH-Px in the cerebellum and cerebral cortex was not significantly different between treated and control animals. The present study demonstrated that developmental BDE-99 exposure causes oxidative stress in the hippocampus of offspring by altering the activity of different antioxidant enzymes and producing free radicals. We demonstrated adverse effects of developmental exposure to BDE-99 associated with tissue concentrations very close to the current human body burden of this persistent and bioaccumulative compound.