Obliteration in Oxidative Stress and Ca++ Uptake in Brain Mitochondria Leads to Impairment of Cholinergic System: A Possible Mechanism Underlying Neurotoxicity Induced by Dichlorvos

Dichlorvos is an organophosphate insecticide effectively used against mushroom flies, aphids, spiders, mites, caterpillars and thrips. Toxicity of dichlorvos is confirmed by air, water and food via inhalation, dermal, absorption and ingestion. Earlier studies velate the dichlorvos administration with the toxicity of the reproductive system, respiratory system, cardiovascular system and nervous system. Primarily, it affects the nervous system through cholinesterase inhibition or anticholinesterase effect and also leads to increased intracellular calcium level, oxidative stress and the rate of lipid peroxidation in the brain mitochondria. Mitochondria are pleomorphic organelles that generate the ATP supply for the cells. Disturbance in the electron transport chain (ETC) of mitochondria by the dichlorvos ultimately increases the ROS production, thereby leading to an increase of oxygen consumption and decrease of ATP synthesis which is the hallmark of the neuronal lesions. The increased calcium level is reported to be associated with neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis. Since, the brain is a controlling and coordinating organ in the body, therefore toxic effects of dichlorvos on it will also be deleterious to other organ-systems indirectly. Current review deals with possible implications of impairment of cholinergic circuit and brain mitochondrial functions carried by dichlorvos which may be the cause of potential neurotoxicity