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Research Article Open Access
Manganese (Mn) is an essential metal that in excess can be toxic especially to brain. Mn exposure in humans and other animals is known to affect central nervous system. Mn access to its toxic target, the brain, is a complex phenomenon subject to physiological and physiopathological processes in which, among others, the route of exposure plays an important role. The brain is the major target organ for Mn toxicity. It retains Mn much longer than other tissues. Following chronic overexposure, Mn can produce a progressive, permanent neurodegenerative disorder, with few options for treatment and no cure. Oxidative stress plays a key role in manganese induced neurotoxicity. Therefore the brain is very susceptible to oxidative stress due to its high oxygen consumption. In the present study Mn was injected intraperitonially (5 mg/kg b.w., i.p. and 10 mg/kg b.w., i.p.) to the male albino rats and oxidative stress enzymes Super oxide dismutase (SOD), Cu/Zn-SOD, Catalase (CAT), Glutathione peroxidase (GPx) were assayed. SOD isoforms, CAT, GPx were decreased significantly in high and low dose of Mn exposure in different brain regions (cerebral cortex, cerebellum and hippocampus) leads to alteration in the activity of antioxidant enzymes. Decrease in antioxidant enzymes were more in high dose compared to low dose. Mn-induced neurotoxicity is both dose and timedependent. Gene expression studies also showed down regulation of Mn- SOD and GPx in dose dependent manner. Our results showed that α-tocopherol expressed protective role against toxic influence of Mn in high and low dose on all examined parameters in rat brain regions.