We have investigated responses of hippocampus Brain Derived Neurotherophic Factor (BDNF) and oxidative biomarkers such as; Total Antioxidant Capacity (TAC) and Malondialdehyde (MDA) to acute treadmill exercise and it’s adaptations to chronic exercise in rats exposed to lead acetate. Forty rats were randomly divided into 5 groups: (1) lead acetate, (2) endurance training, (3) acute training, (4) endurance+ acute training and (5) sham groups. Groups 1 to 4 received lead acetate (20 mg/kg), while sham group received ethyl oleat (30 mg/kg), intraperitoneally. The rats in groups 2 and 4 experienced the treadmill running for 8 weeks (15-22 m/min, 25-64 min) and the subjects in groups 3 and 4 ran on the treadmill at 1.6 km/h until exhaustion, immediately before death. Lead administration decreased BDNF, insignificantly and TAC, significantly and caused a significant increased in MDA. In contrast, performing 8 weeks exercise enhanced the hippocampus BDNF and plasma TAC, significantly and reduced MDA, which was significant in plasma. On the other hand, both acute exercises caused increased in BDNF, plasma MDA and decreased hippocampus MDA, while one bout of acute exercise enhanced TAC, endurance+ acute exercise reduced TAC, significantly. The findings of this study imply that chronic exercise seems to produce benefits more reliably and suggest as lifestyle-induced neuroprotective potential in ameliorating lead-induced neurotoxicity.
Keywords: endurance exercise, acute exercise, lead, neurotoxicity, BDNF, oxidative stress