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Abstract:We investigated the effect of aluminium phosphide exposure (10 mg/kg body weight) on lipid peroxidation and antioxidant defence system in different regions of rat brain. A significant increase in lipid peroxidation in cerebrum, cerebellum and brain stem was observed in aluminium phosphide-exposed rats, which was accompanied by a marked decrease in the activities of antioxidant enzyme, superoxide dismutase and catalase. A decline in the activity of glutathione reductase was also observed, however, no change was seen in the activity of glutathione peroxidase following aluminium phosphide administration. Decreased levels of non-protein thiols and total sulfhydryl groups were also observed after aluminium phosphide treatment. It seems evident that aluminium phosphide exposure significantly enhanced neuronal lipoperoxidative damage with concomitant alterations in the antioxidant defence status thus having serious bearing on the functional and structural status of the central nervous system.

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The effects of lead (Pb) and selenium (Se) interactions on central nervous system (CNS) functions were seen in adult rats by both biochemical and histologic pathological alterations. Pb administration of 20 mg/kg body wt for 8 wk showed degenerative changes only in the cerebral cortex. The changes in the cerebellar regions were not significant. Biochemically a marked decrease in the DNA, RNA, and protein content was seen following lead treatment. These decreases were significant in both the regions of the brain. During the concomitant administration of Pb and Se, the alterations in the transverse section of cerebral cortex showed only marginal changes. The values of DNA and RNA content showed significant improvement in both regions of the brain compared to the Pb treated group.