Objective To explore the effect of vitamin E (VE) against the neurotoxicity of benzo[a]pryene (B[a]P) in male SD rats. Methods A total of 60 male SD rats were randomly assigned to one of the following six groups (n=10/group): the blank control group, vehicle control group, B[a]P group(5 mg/kg), low dose of VE (10 mg/kg) + B[a]P (5 mg/kg) group, medium dose of VE (50 mg/kg) + B[a]P (5 mg/kg) group and high dose of VE (100 mg/kg) + B[a]P (5 mg/kg) group. The rats were gavaged with the corresponding dose of B[a]P once a day for 30 days. Morris water maze was used to evaluate the learning and memory performance of rats. Morphological changes in hippocampus were observed. The activities of superoxide dismutase(SOD), glutathione peroxidase(GSH-Px) and γ-glutamylcysteine synthetase(γ-GCS), the contents of glutathione(GSH), oxidized glutathione (GSSG) and malonaldehyde (MDA) in the hippocampus tissue were all examined. Results The results of the behavior tests showed that rats treated with B[a]P exhibited a significantly increased escape latency and a significantly decreased cross-platform times and the residence time on the platform compared with the blank control group and vehicle group (P<0.01). VE treatment could obviously improve the changes of the above index (P<0.01). Besides, the morphological changes in hippocampus suggested that VE could protect against the injury induced by B[a]P. The activities of SOD, GSH-Px and γ-GCS and the contents of GSH, GSSG in rat hippocampus of B[a]P group were significantly decreased, while the content of MDA was significantly increased compared with the blank control group and vehicle control group (P<0.01). Moreover, the above indices were obviously improved with the increase of VE dosage in VE groups. Conclusion VE can play an protective role in B[a]P-induced neurotoxicity.