1 research outputs found
Arsenic-Induced Mitochondrial Instability Leading to Programmed Cell Death in the Exposed Individuals
InWest Bengal, India, more than 6 million people in nine districts are exposed to arsenic through drinkingwater. It is regarded as the greatest arsenic
calamity in the world. Arsenic is a well-documented human carcinogen, which does not induce cancer in any other animal model. Interestingly,
at lower concentrations, arsenic is known to induce apoptosis in various cancer cell lines in vitro. We have studied apoptosis in human peripheral
blood mononuclear cells (PBMC) of 30 arsenic exposed skin lesion individuals by annexin V-FITC staining and compared with 28 unexposed
individuals. The percentage of apoptotic cells in individuals with skin lesions was significantly higher (p < 0.001) in comparison to unexposed
individuals. In the exposed individuals with skin lesions, there were elevated levels of intracellular reactive oxygen species (ROS), mitochondrial
membrane permeability and increased cytochrome c release, leading to increased downstream caspase activity. Arsenic-induced DNA damage was
confirmed by DNA ladder formation and confocal microscopy. We also observed that chronic arsenic exposure reduced Bcl-2/Bax ratio and also
resulted in cell cycle arrest of PBMC in G0/G1 phase. All these observations indicate that mitochondria-mediated pathway may be responsible for
arsenic-induced apoptosis