STUDY OF THE NEUROPROTECTIVE EFFECT OF ALPHA LIPOIC ACID ON ACRYLONITRILE INDUCED CELLULAR & MITOCHONDRIAL DYSFUNCTION BY ENHANCEMENT OF OXIDATIVE STRESS IN RAT HIPPOCAMPUS MAPPING.

Acrylonitrile, one of the nitrile derivatives causes neurotoxicity. It has been suggested that mechanism involved can be generation of free radicals and mitochondria play an important role in this process. It has been reported that ALA (Alpha lipoic acid) by the virtue of its antioxidant nature may prevent free radical induced neurotoxicity. In this work, we investigated the effects of Acrylonitrile (50mg/kg body weight) and Alpha lipoic acid (100mg/kg body weight) on hippocampal cellular and mitochondrial enzyme activities such as SOD (superoxide dismutase), GPx (glutathione peroxidase), CAT (catalase) and GSH (reduced glutathione) and MnSOD (manganese Superoxide dismutase), GPx, GST (glutathione-s-transferase) and GSH respectively. Moreover, we also studied the damage on mitochondrial membrane by measuring MDA (malondialdehyde) level. The activities of TCA cycle enzymes such as ICDH (isocitrate dehydrogenase), SDH (succinate dehydrogenase), ?-KDH (Alpha ketoglutarate dehydrogenase) and MDH (malate dehydrogenase) were significantly reduced after Acrylonitrile administration. Subsequent treatment with ALA significantly alleviated the depletion in the level of these enzymes. We measured the activities of ETC enzymes NADH dehydrogenase and Cytochrome C oxidase. Acrylonitrile administration significantly down regulated the activities of these enzymes whereas ALA restored the levels of these enzymes. In conclusion, our data indicate that ALA effectively protects the hippocampal cellular and mitochondrial damage provoked by Acrylonitrile.