PAN AFRICAN JOURNAL OF LIFE SCIENCES
Volume 5, No. 2, August 2021
Synergetic Treatment of Ascorbic Acid and Nicotine Ameliorates Aluminium Induced Neurotoxicity in the Prefrontal Cortex of Wistar Rat
Taiwo A. Abayomi1*, Olorunfemi S. Tokunbo1, Temilola D. Olawore1, Olawale A. Abayomi2, Ajilore S. Bamidele3, Abiodun Akinyemi1
1Department of Anatomy, Faculty of Basic Medical Sciences, College of Health Sciences, Osun State University, PMB 4494, Osogbo, Osun State, Nigeria.
2Department of Radiology, Faculty of Clinical Sciences, Ekiti State University, Ekiti State, Nigeria
3Department of Biochemistry, Faculty of Basic Medical Sciences, College of Health Sciences, Osun State University, PMB 4494, Osogbo, Osun State, Nigeria
Background: Though the neuroprotective roles of ascorbic acid are well established, the therapeutic role of nicotine in various neurological disorders is attracting increasing attention. This study evaluated the putative ameliorative role of the synergetic treatment of nicotine and ascorbic acid against neurodegenerative consequences associated with free radical species and amyloid plaques generation in adult male Wistar rats
Methods: A total of 35 Wistar rats were distributed into five groups labeled A-E. Group A served as the control group; animals in group B were treated with 100mg/kg body weight of aluminium chloride (AlCl3) for 21 days. Group C animals were treated with 100mg/kg body weight of aluminium chloride for 21 days and post-treated with 14mg/kg body weight of nicotine for 21 days. Group D was treated with 100mg/kg body weight of aluminium chloride for 21 days and post-treated with 100mg/kg bodyweight of ascorbic acid for 21 days. Group E animals were treated with 100mg/kg body weight of aluminium chloride for 21 days and post-treated with 100mg/kg bodyweight of ascorbic acid and 14mg/kg body weight of nicotine. On completion of treatments, the prefrontal cortex was excised and processed for biochemical and histochemical examinations.
Results: Oxidative stress was evident from the diminished level of catalase and glutathione per oxidase and elevated lipid peroxidation levels in animals administered with aluminium in addition to the presence of amyloid plaques in these animals. However, synergetic administration of ascorbic acid and nicotine attenuated these oxidative and histochemical perturbations induced by aluminium.
Conclusion: Synergetic treatment with ascorbic acid and nicotine provided better ameliorative potential against aluminium-induced neurotoxicity compared to either ascorbic acid or nicotine treatments alone
Keywords: Neurotoxicity, Ascorbic acid, nicotine, amyloid plaques, oxidative stress