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ABSTRACT
The recent surge in the worldwide incidence of neurodegenerative disorders has been linked to an escalation in the presence and dissemination of harmful chemicals within the biological ecosystem through contamination of water, air and food sources. This phenomenon has resulted in more than 46.8 million individuals experiencing dementia and a multitude of other health related issues on a global scale. The recognition of the toxic nature of lead (Pb) and aluminium (Al) to various organisms, including humans, dates back to a considerable period in history. Although Pb and Al can be distributed throughout various organs within the human body, the central nervous system stands out as a primary focal point for the adverse consequences associated with both of these metals. There is paucity in literature evidence to histologically demonstrate the deleterious effects of Pb and Al in the cerebrum and hippocampus of experimental animals. Accordingly, this study was designed to investigate such activity. A total of twenty-one (21) Wistar rats weighing between 120 g to 160 g were used in this study. After acclimatization, the rats were randomly assigned to three groups (A, B and C) of seven rats each. All administrations were consumed orally by an orogastric tube which lasted for 28 days and the rats were fed standard rat chow throughout the entire study period. Group A rats served as the control group and were given 1 ml of distilled water. Group B rats were administered 100 mg/kg body weight of Lead Acetate only. Group C rats were administered with 100 mg/Kg body weight of Aluminium Chloride only. At the end of the experiment, the animals were weighed and an assessment of neurobehavioural activities (Ymaze, Novel Object Recognition (NOR) and Elevated Plus Maze tests) was conducted. Subsequently, the rats were sacrificed and the cerebrum and hippocampus were harvested to investigate antioxidant activity and histological alterations. Results showed a significant decrease (p< 0.05) in final body and brain weight of rats treated with lead acetate and aluminium chloride in contrast to the control which was significantly higher. Comparison of neurobehavioural activity showed that rats in the Pb and Al group had significantly reduced (p< 0.05) neurobehavioral function (reduced discrimination index, spontaneous alternation and increased transfer latency) compared to those in the control. Assessment of antioxidant activity by (SOD, CAT, GSH and GPx) showed oxidative stress (low antioxidant activity and elevated lipid peroxidation) in the cerebrum and hippocampus in the Pb and Al groups whereas the control group had significantly higher antioxidant activity and reduced lipid peroxidation. Histological findings revealed morphological alterations (several dark shrunken neuronal cell bodies with deeply stained pyknotic nuclei in the cerebrum and atrophy of pyramidal cells and astrocytes and vacuolations in the hippocampus) in the Pb and Al group while the control group had normal morphology/histoarchitecture. Taken together, Pb and Al were neurotoxic to the Wistar rats and consequently, this study helps to improve comprehension of heavy metal poisonings and its deleterious effect in the brain.
