ABSTRACT
Aluminum chloride (AlCl3), known for its neurotoxic properties, disrupts both the structure and operations of the hippocampus, including its capacity for neurogenesis, ultimately resulting in cognitive and memory deficiencies. Aluminum chloride (AlCl3) also causes deficiencies in spatial memory, emotional responsiveness, and cognitive brain function impairments. Ascorbic acid also known as Vitamin C is a key antioxidant which plays an essential role in numerous physiological processes. It is advantageous in the rejuvenation of neurons damaged by conditions such as ischemia and neuronal inflammation. Ascorbic acid additionally provides protection against the development of diverse neurodegenerative conditions like Parkinson’s disease, Alzheimer’s disease and stroke. Accordingly, this study was designed to investigate the antioxidant and anticholinesterase activity of ascorbic acid in the hippocampus of Wistar rats treated with Aluminium chloride. After purchase and acclimatization, the Wistar rats were weighed and divided into six equal groups (control and treatment groups). Group A (Control) was administered 1 ml dH2O/day. Group B (AlCl3) was administered 100 mg/kg body weight (BW) of Aluminium chloride only. Group C (AlCl3 ＋ AA1) was administered 100mg/kg body weight of Ascorbic acid and Aluminium chloride. Group D (AlCl3 ＋ AA2) was administered 200mg/kg body weight of Ascorbic acid and Aluminium chloride. Group E (AA1) was administered 100mg/kg body weight of Ascorbic acid. Group F (AA2) was administered 200mg/kg body weight of Ascorbic acid. Administration lasted for 28 days and was done via an orogastric tube, Aluminium chloride (AlCl3) was administered one hour before Ascorbic acid (AA). The rats were fed with standard rat chow and had free access to water throughout the entire study period. Animals were weighed every two weeks before commencement and throughout the experiment. At the end of the experiment, neurobehavioral activity (y- maze test) was evaluated, recorded, and the rats were then sacrificed for sample collection. Following appropriate harvesting of the hippocampus, the antioxidant activity [Catalase (CAT), Glutathione Peroxidase (GPx), Superoxide Dismutase (SOD), Glutathione (GSH)] and Lipid Peroxidation (MDA) were evaluated. Also, The Acetylcholinesterase (AChE) activity and histological alterations were investigated. The results showed a significant decrease in final body weight (FBW) of rats in the AlCl3 group in contrast to the control and pre-treated AA groups which showed a higher FBW. Comparison of neurobehavioral activity (y- maze test) showed that rats in the AlCl3 group had significantly reduced neurobehavioral function compared to those in the control and pre-treated AA groups. Assessment of antioxidants (SOD, CAT, GSH, GPx) showed low antioxidant activity and elevated Lipid peroxidation in the hippocampus of AlCl3 group whereas in the Control and pre-treated AA groups there was a significantly higher antioxidant activity and a lower Lipid peroxidation. Histologically findings showed structural alterations in the hippocampus of rats treated with AlCl3 alone (atrophy and vacuolated pyramidal cells and astrocytes). While the pre-treated groups showed similar morphology to the control groups. In conclusion, the findings showed that AA was not toxic to the animals but protected against AlCl3 toxicity. The findings from this study provide the first research evidence on the protective activity of Ascorbic acid against Aluminium chloride-induced neurotoxicity in Wistar rats.
