Neuroprotective potential of N -acetylcysteine in carbofuran neurotoxicity: A biochemical and histopathological study

The present study was undertaken to evaluate biochemical markers of chronic carbofuran exposure to rats in terms of lipid peroxide and intrasynaptosomal calcium levels and to correlate them with the histopathological changes in brain regions. A significant increase in lipid peroxidation (LPO) in terms of thiobarbituric acid reactive substances (TBARS) was observed in the cerebral cortex (65%) and brain stem (33%) after carbofuran exposure. This was accompanied by a significant increase (87%) in the intracellular free-Ca²⁺ [Ca²⁺]_i levels. N-acetylcysteine (NAC) administration, on the other hand, reversed the carbofuran-induced increase in LPO and [Ca²⁺]_i. Histopathological studies of carbofuran-exposed brain revealed high frequency of pyknotic neurons in the cerebral cortex and microhaemorrhages in the brain stem. NAC supplementation to carbofuran-treated animals resulted in normalisation of the brain architecture as seen by a reduction in the number of pyknotic nuclei in the cerebral cortex. These findings indicate that increased LPO and elevated [Ca²⁺]_i levels are involved in the development of carbofuran neurotoxicity and are eventually responsible for the pathological alterations. The study also demonstrates potential neuroprotective effect of NAC treatment in carbofuran neurotoxicity.