Evaluation of The Effect of Environmental Toxins on Neuronal Functions

Abstract

Background and objective Neurodegenerative disorders are characterized by progressive and irreversible loss of neurons in the specific region of brain. Alzheimer disease is the neurodegenerative disease in which destruction of brain cells leading to dementia. Oxidative stress and mitochondrial DNA mutation are both contributing to the aging process and that is the greatest risk factor responsible for neurodegeneration. Exposure to environmental toxins like aluminium chloride which leads to the condition like neuronal degeneration. Aluminium chloride produces oxidative damage by the process of apoptosis, increasing oxidative stress that can cause formation of reactive oxygen species (ROS). ROS generation activates the inflammatory response and leads to neuronal degeneration. Sodium azide is also acutely toxic environmental toxin. It is metabolized into the liver and enters into the blood brain barrier. Azide ions metabolized to nitric oxide (NO). This nitric oxide is responsible for toxic effects. Sodium azide is producing mitochondrial dysfunction. It is a specific inhibitor of cyclooxygenase (COX). This inhibition increases the production of ROS and produces neurotoxicity. The aim of the present study was to evaluate the effect of aluminium chloride (AlCl3) and sodium azide (NaN3) on neuronal functions and to find out pathogenic mechanism for that.Material and Methods In the present study, after acclimatization and training wistar rats were divided in six groups namely normal control (NC), disease induced with aluminium chloride (Al100), disease induced with sodium azide (NA5), disease induced with sodium azide (NA10), disease induced with aluminium chloride and sodium azide (Al+NA5) and disease induced with aluminium chloride and sodium azide (Al+NA10). Alzheimer’s disease was induced by aluminium chloride (100mg/Kg, p.o.) for 28 days, NA5 and NA10 groups received sodium azide (5 mg/kg, s.c. and 10mg/kg, s.c.) for 12 days and 7 days respectively. Al+NA5 and Al+NA10 groups received aluminium chloride (100mg/kg) for 28 days after that Sodium azide (5mg/kg and 10mg/kg) form 29th day to 40th day and from 29th day to 35th day respectively. Normal control animals received distilled water. Furthermore, rats were given training on water maze and radial arm maze to check the behavioural pattern and were assessed once a week till 5 weeks using radial arm maze and water maze from 35th day to 40th day. On the 40th day, after the last dose, animals were sacrificed, blood was collected and the brain was isolated to check biochemical and histopathological changes.