Title : Neuroprotective effect of Alpha Lipoic Acid on neurotoxicity induced by nitrile derivatives
Nitrile derivatives are known to cause toxicities like neurotoxicity, hepatotoxicity, cardiovascular, renal and gastrointestinal disorders. Nitriles collates a broad range of chemicals including Acetonitrile, Acrylonitrile, Butyronitrile, Valeronitrile etc. widely utilized in different manufacturing industries and materials. Mitochondria and free radical generation are indicated to play a crucial role in the mechanism and uplifting the biological effects of induced toxicities. Alpha lipoic acid (ALA) is reported to be efficient enough to inhibit and prevent free radical generation persuaded toxicity because of its antioxidative activity. In this study, we investigated the effects of nitrile derivatives and Alpha lipoic acid (ALA) on hippocampal cellular and mitochondrial enzyme activities such as SOD (superoxide dismutase), GPx(glutathione peroxidase), CAT (catalase) and GSH (reducedglutathione) and MnSOD (manganese Superoxide dismutase), GPx,GST (glutathione-s-transferase) and GSH respectively. We also studied the effects and alterations caused by nitrile derivatives administration on the enzymes of TCA cycle and mitochondrial membrane. In this study, damage in mitochondrial membrane and significant reduction in the enzymatic activities of TCA Cycle such as ICDH (isocitrate dehydrogenase), SDH (succinate dehydrogenase), α-KDH (Alpha ketoglutarate dehydrogenase) and MDH (malate dehydrogenase) was observed. Considerable downfall in the levels of these enzymes was observed on subsequent treatment with Alpha Lipoic Acid (ALA). Activities of ETC enzymes NADH dehydrogenase and Cytochrome C oxidase were also studied, where nitrile derivatives were found to downregulate the enzymatic action. It is hereby concluded that whilenitrile derivatives demonstrated toxicities by altering enzymatic activities and damaging mitochondrial membrane, Alpha lipoic acid (ALA) restored the altered enzymatic action and efficiently preserved the hippocampal cellular and mitochondrial damage induced by nitrile derivatives.