Biochemical and ultrastructural evidences for toxicity of lead through free radicals in rat brain.

Studies suggest that some lead-induced toxic effects may occur through free radical production and oxidative stress. This study examined the relationship between brain histopathological alterations and oxidative stress in subchronic lead exposure. Male Albino rats received lead acetate at 0.01%, 0.05% and 0.1% w/v in their drinking water for 30 days. Animals given sodium acetate (0.1% w/v) served as control in the same period. At the end of exposure, blood-lead levels, blood catalase (CAT) and superoxide dismutase (SOD) activities and malondialdehyde (MDA) content (in blood and brain) were measured. The brain tissue samples were prepared and analysed by light and scanning electron microscopy. The results show that, the blood-lead levels in treated animals were higher in comparison with control. CAT and SOD activities in animals treated with 0.01% and 0.05% w/v did not increase in comparison with control (P > 0.05) but these values were higher in animals treated with 0.1% w/v lead acetate (P < 0.01). MDA content in blood and brain of animals treated with lead acetate 0.1% w/v, increased significantly (P <0.01), but these values were not significantly increased in other treated animals. No major histopathological alterations were detected in the brains of animals treated with lead acetate at 0.01% and 0.05% w/v. In animals treated with lead acetate 0.1% w/v, demyelinization and collagenous scar formation with neuronal atrophy in hippocampus region was observed. It is concluded that lead acetate induce oxidative stress which has an important role in brain damage in rats.