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After intraperitoneal injection of 20 mg/kg lead acetate, rats received 8 weeks of treadmill exercise (15-22 m/min, 25-64 minutes) and/or treadmill exercise at 1.6 km/h until exhaustion. The markers related to neurotoxicity were measured by enzyme-linked immunosorbent assay method. 8 weeks of treadmill exercise significantly increased brain-derived neurotrophic factor level in the hippocampus (P = 0.04) and plasma level of total antioxidant capacity of rats exposed to lead acetate (P < 0.001), and significantly decreased plasma level of malondialdehyde (P < 0.001). Acute exercise only decreased the hippocampal malondialdehyde level (P = 0.09) and increased brain-derived neurotrophic factor level in the hippocampus (P = 0.66). Acute exercise also enhanced the total antioxidant capacity in rats exposed to lead acetate, insignificantly (P = 0.99). These findings suggest that chronic treadmill exercise can significantly decrease neurotoxicity and alleviate oxidative stress in rats exposed to lead acetate. However, acute endurance exercise was not associated with these beneficial effects.(1) We investigated the effects of acute endurance exercise and chronic exercise at low intensity on lead acetate-induced neurotoxicity and oxidative stress.(2) Acute endurance exercise was associated with lower induction of brain-derived neurotrophic factor in the hippocampus of rats exposed to lead acetate compared with chronic exercise.(3) Chronic exercise increased total antioxidant capacity, but acute exercise had no effect.(4) Chronic exercise greatly decreased the plasma level of malondialdehyde, while acute endurance exercise had no such effect.(5) Exercise training can improve brain resistance to neurodegenerative diseases induced by air pollutants.