Normal cellular metabolism produces oxidants that are neutralized by the cells' antioxidant enzymes and antioxidants taken from outside. An imbalance between oxidant and antioxidant has been postulated to lead to the neurodegeneration in the ischemic condition. In this study, we have demonstrated the prevention or slowdown of neuronal injury in middle cerebral artery occlusion (MCAO) by sodium selenite. Rats were pretreated with 0.05, 0.1, and 0.2 mg/kg body wt of sodium selenite for 7 d. The rats of group I (sham) and group II (ischemia) were pretreated with physiological saline for 7 d. On d 8, MCAO was induced for 2 h in the right side of brain of group II, III, IV, and V rats. Brains were dissect out after 22 h of reperfusion and washed with chilled physiological saline. The right cerebral hemisphere was used for the preparation of mitochondria. The activity of superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, and monoamine oxidase (MAO-A and MAO-B) was depleted significantly; conversely, the activity of poly(ADP-ribosyl) polymerase was elevated significantly as compared to the sham, and the pretreatment of the animals with different doses of sodium selenite has protected the activity of these enzymes significantly. The content of glutathione was decreased significantly, whereas the level of lipid peroxidation was increased significantly in the mitochondria of MCAO as compared to the sham group, and pretreatment with different doses of sodium selenite has protected their levels significantly as compared to the MCAO group. It is concluded that selenium, which is an essential part of our diet, might be helpful in protection against neurodegeneration in cerebral ischemia.

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The effect of 0.05, 0.1, and 0.2 mg sodium selenite/kg body weight ip on the activities of neurobehavioral, acetyl cholinesterase, monoamine oxidase, and the content of dopamine and its metabolites in circadian rhythm centers of male Wistar rats was studied after 7 d of treatment. The results show an appreciable increase in locomotion, stereo-events, distance traveled, and average speed at the dose of 0.1 and 0.2 mg sodium selenite/kg. The data have shown hyperactivity of animals with various doses of sodium selenite, and it was significant and dose-dependent after 3 d of treatment. The activity of acetylcholinesterase (AChE) was inhibited dose dependently, and it was significant in preoptic area with 0.1 or 0.2 mg sodium selenite/kg. Conversely, in the posterior hypothalamus its activity was significantly elevated with the dose of 0.2 mg sodium selenite/kg, but its alteration in brain stem was not significant. Monoamine oxidase (MAO) activity was increased in preoptic area with the dose of 0.1 mg sodium selenite/kg, but its alteration in posterior hypothalamus and brain stem was not significant. The content of dopamine (DA), 3,4-dihydroxyphenyl acetic acid (DOPAC), and homovanilic acid (HVA) was elevated dose dependently and it was significant with the doss of 0.1 and 0.2 mg sodium selenite/kg, but the content of DOPAC and HVA in posterior hypothalamus was not significant with the dose of 0.1 mg sodium selenite/kg.