Environmental toxins and Parkinson’s disease: Putative roles of impaired electron transport chain and oxidative stress

Abstract

Despite recent advancements in the biomedical fields, the etiology and pathogenesis of Parkinson’s disease (PD) is still poorly understood, though the crucial roles of oxidative stress and impaired mitochondrial respiration have been suggested in the development of PD. The oxidative modification of the proteins of mitochondrial electron transport chain alters their normal function leading to the state of energy crisis in neurons. Exposure of environmental chemicals such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and rotenone in mouse produces the symptoms akin to PD and therefore these neurotoxins are commonly used in experimental studies on PD. Another environmental toxin, paraquat (a commonly used herbicide) has also been implicated with the onset of PD. The neurotoxicity of these chemicals is accompanied by the blockade of electron flow from NADH dehydrogenase to coenzyme Q. The agents with the ability to improve mitochondrial respiration and ATP production have been shown to exert beneficial effects in PD patients as well as in the animal models of PD. This review summarizes the current research implicating the impairment of mitochondrial respiratory chain and the role of environmental toxins in the pathogenesis of PD.