THE NEUROPROTECTIVE ROLE OF NICOTINE AND ASCORBIC ACID ON ALUMINIUM CHLORIDE (ALCL3)-INDUCED NEUROTOXICITY IN THE HIPPOCAMPUS OF ADULT MALE WISTER RATS.

ObjectivesFree radicals induced oxidative stress has been disrupted in the neurological functionality of the hippocampus in relation to aluminium chloride induced neurotoxicity. Ascorbic acid was been used as an antioxidants to prevent the oxidative damage induced by aluminium chloride. Therefore this present study was conducted to evaluate the antioxidant role Ascorbic acid and nicotine against the neurodegenerative consequences associated with aluminium chloride. Materials and methodThirty five (35) adult male Wister rats weighing 130-150g per body weight was used for this study. The rats were randomly grouped into five groups (A, B, C, D, and E) with each group having seven animals. Animals in group A(control group) were fed only water ad libitum for 21 days; animals in group B were administered Aluminium Chloride only with 100mg/kgBW for 21 days; animals in group C were administered aluminium chloride for the first 21 days with 100mg/kgBW, after which nicotine of 14mg/kgBW was administered. Animals in group D was administered with aluminium chloride of 100mg/kgBW for the first 21days after which Ascorbic acid was administered with 100mg/kgBW for the next 21days. Animals in group E were administered with Aluminium chloride, received 100mg/kgBW of Alcl3 for the first 21days then 14mg/kgBW Nicotine for 21days follow by administration of 100mg/kgBW of Ascorbic acid for the next 21days, concomitantly. ResultsOxidative stress was observed from the degeneration the antioxidants (catalase, glutathione peroxidase, superoxide dismutase) in animals that were exposed to aluminium chloride. Histological examination showed that the hippocampus microarchitecture of animals exposed to aluminium chloride have a neurodegenerative changes characterized fragmentation, chromatolytic changes as well as some pyknotic changes in the purkinje and granule cell layers with a gross reduction in the cytoplasmic Nissl proteins. Administration of Ascorbic acid and nicotine was said to revert close to all the cytoarchitectural, biochemical, neurochemical, and immunohistochemical alterations induced by aluminium chloride neurotoxicity. ConclusionThe results suggests that the administration of Ascorbic acid and nicotine may have caused a significant ameliorative effect against the neurotoxicity of aluminium chloride.