This study was planned to determine the influence of age on arsenic (As; 10mg/kg body weight given through oral gavage) induced mitochondrial oxidative stress in three different age groups of rats; young (postnatal day [PND] 21), adult (3 months) and aged (18 months) at seven days post-acute exposure. Further, we also evaluated the therapeutic efficacy of essential metal Zinc (Zn; 0.02% through drinking water) and an antioxidant, α-Tocopherol (Vit-E; 125mg/kg body weight through oral gavage) against As-induced neurotoxicity. As exposure lead to a significant decrease in mitochondrial Superoxide Dismutase isoforms (Mn-SOD and Cu/Zn-SOD), Catalase (CAT), Glutathione reductase (GR), Glutathione peroxidase (GPx), non-enzymatic antioxidant levels of glutathione (GSH), total free sulfhydryl groups (TSG) with concomitant increase in lipid peroxidation and GST in different brain regions (cerebral cortex, cerebellum and hippocampus) of different age groups of rats. These effects were more pronounced in cerebral cortex followed by cerebellum and hippocampus. Among the three different age points, aged animals were found to be more vulnerable to the As-induced toxicity as compared to young and adult animals suggesting that As neurotoxicity is age dependent. These As-induced alterations were significantly reversed following supplementation with Zn or Vit-E. However, Vit-E was found to elicit greater protection as compared to Zn in restoring the altered neurochemical perturbations, providing evidence for As induced oxidative damage.
Age, Arsenic, Zinc, Vitamin-E, Oxidative stress, Brain regions
