Effect of Long Term Administration of Aluminium Chloride on Oxidative Stress and Acetylcholinesterase Activity in Rat Brains

Oxidative modifications are the hallmark of oxidative imbalance in the brain of individuals with Alzheimers, Parkinsons and Prion diseases and their respective animal models. The aim of the research was to study the impact of aluminum chloride (AlCl3) administration in drinking water (7mg/kg body weight) and Dgalactose(i.p).The results revealed that the levels of lipidperoxidation were significantly increased, while the activities of superoxide dismutase (SOD) as well as reduced glutathione (GSH) content were significantly decreased in the brains of rats. Additionally, brain acetylcholinesterase (AChE) activities were significantly increased. It can be concluded that Al-induced neuronal oxidative stress and inhibition of the antioxidant system and enzyme activities could be the mechanisms of AlCl3 neurotoxicity. The stained samples were examined by means of light microscope for histological changes. Histological examinations showed clumpy of cell neurons, or reduced pyramidal cells and scanty neurofibrillary tangle which was an indication of neurodegeneration in the treated groups when compared to the control. It was however, concluded that the oral administration of aluminium chloride could induce brain damage which may impair memory and learning as seen in Alzheimer disease.These results suggest that AlCl3, enhances oxidative stress in the brain, thereby disturbing the antioxidant defense of rats. Increased oxidative stress could be one of the mediating factors in the pathogenesis of AlCl3, toxicity in the brain.