Changes in neurotrophic factor and oxidative stress induced by lead in rat brain
For many years it has been known that lead is life-threatening, not only as an air pollutant but also because of it has been associated with several conditions including degenerative disease of the nervous system. In the current study we investigated neuroprotection effects of exercise training and/or curcumin on lead acetate-induced neurotoxicity in the rat hippocampus. Forty rats were randomly divided into five groups: 1) lead acetate, 2) curcumin, 3) endurance training, 4) training+curcumin, and 5) sham. The rats in the training groups performed treadmill running consisting of 15 to 22 m/min for 25 to 64 min, 5 times a week for 8 weeks. All groups except sham received lead acetate (20 mg/kg), whereas the sham group received curcumin solvent. In addition, the curcumin and training+curcumin groups received curcumin solution (30mg/kg) intra peritoneally. Chronically administration of lead acetate resulted in a significantly increase in the malondialdehyde (MDA) in plasma, but not in hippocampus. In addition, it led to significantly decreased brain-derived neurotrophic factor (BDNF) in hippocampus and total antioxidant capacity (TAC) levels, as compared to sham group. Treadmill running, curcumin supplementation, or both resulted in a significant decrease in MDA levels and significantly increased BDNF and TAC levels, as compared to lead acetate group. These results provide a rationale for an inhibitory role of curcumin and regular exercise in the attenuation of lead-induced neurotoxicity.