ARSENIC AND ITS MITOCHONDRIAL TOXICITY: A REVIEW

The present review article deals with environmental origin of arsenic (As) and its oxidative stress mediated mitochondrial toxicity of arsenic. It is a metalloid compound occurs naturally, being the 20th most abundant element in the earth’s crust, and is a component of more than 245 minerals. The presence of As in the environment may be due to both natural and anthropogenic sources. The symptoms of As toxicity either through consumption of contaminated ground water or food crops. The toxicity of As compounds depends on a number of factors. Mostly inorganic trivalent form of Asarsenite (AsIII) is more toxic than arsenate (AsV). Reactive oxygen species (ROS)-mediated oxidative damage is a common denominator in As pathogenesis. In addition, arsenic induces morphological and molecular changes in the integrity of mitochondria through ROS mediated oxidative stress. Further the mechanisms of free radical formation derived from the superoxide radical, combined with glutathione-depleting agents, increase the sensitivity of cells to arsenic toxicity because of its sulfhydryl groups (SH). Finally this review article included origin of ‘As’ and oxidative stress mediated mitochondrial toxicity to address the ‘As’ induced mechanism of mitochondrial dysfunction