Abstract: Objective To observe the effects of lead exposure through drinking water on the expression of APE1 pro⁃ tein in cerebral cortex, cerebellum and hippocampus of rats and its relationship with oxidative stress. Methods Forty weaned male SD rats were randomly assigned to five groups (control group and four exposure groups) according to body weights of rats. Rats in control group were given deionized water as drinking water. Rats in four exposure groups were given 100 mg/L, 200 mg/L, 400 mg/L and 800 mg/L lead acetate solution for 60 days. The activity of superoxide dismutase (SOD), the contents of hydrogen peroxide (H2O2) and malondialdehyde (MDA) in cortex, cerebellum and hippocampus were measured using kits. The protein level of APE1 in cortex, cerebellum and hippocampus were detected by Western blotting assay. Results After being exposed to lead, the APE1 protein levels were significantly decreased in cortex, cerebellum and hippocampus (P < 0.05). The protein level showed a trend of gradual decline with the increase of exposed lead (P < 0.05). With the increase of dye lead dose, the activity of SOD in cortex, cerebellum and hippocampus showed a downward trend, while the contents of H2O2 and MDA showed a rising trend. The activity of SOD was positively correlated with APE1 protein level in cortex, cerebellum and hippocampus (r=0.619, 0.380 and 0.375， P < 0.05). While the contents of H2O2 and MDA were neg⁃ atively correlated with APE1 protein level in cortex, cerebellum and hippocampus (r=-0.472, -0.535, -0.436, -0.514, -0.486 and - 0.316， P < 0.05). Conclusion Lead exposure through drinking water can affect the expression of APE1 protein through inducing oxidative stress in brain tissues of rats.

Key words: lead, brain tissue, oxidative stress, APE1, superoxide dismutase, hydrogen peroxide, malonaldehyde