Objective To investigate the protective effects of vitamin E (VE) on benzo(a)pyrene (B[a]P)-induced liver toxicity in male Sprague Dawley (SD) rats and to discuss the potential mechanisms involved. Methods Sixty male SD rats were randomly divided into 6 groups, namely, the blank control group, vehicle control group, B[a]P group (5 mg/kg), VE (10 mg/kg) + B[a]P (5 mg/kg) group, VE (50 mg/kg) + B[a]P (5 mg/kg) group and VE (100 mg/kg) + B[a]P (5 mg/kg) group, with each group having 10 rats. The rats were treated with B[a]P and/or VE once a day for 30 days via intragastric administration, and then the levels of alanine aminotransferase (ALT), aspertate aminotransferase (AST), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), 8-hydroxy-2-deoxyguanosine (8-OHdG), malondialdehyde (MDA) and tumor necrosis factor-α (TNF-α) were determined. The morphological changes of liver tissue were observed by H-E staining. Results Compared with the blank control group, the liver tissues in the B[a]P group were injured, the activities of serum AST, ALT, and the levels of MDA, 8-OHdG and TNF-α in B[a]P group were increased significantly (P<0.05); however, the activities of SOD and GSH-Px were significantly decreased (P<0.05). Importantly, rats in VE treatment groups had attenuated injury to liver tissues to different extents, decreased aminotransferase levels and greatly improved oxidative and DNA injury indicators. And with the increase of VE dose, the protective effect was more potent. Conclusion VE has a protective effect against the B[a]P-induced liver toxicity in male SD rats.