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Arsenic poisoning is one of the major devastation and horrific concerns across the globe. Its concentration in the environment is continuously increasing over time, and hence it may play a role of exterminator for the future civilization. Cancer is the one of the main detrimental outcomes of arsenic poisoning. The International Agency for Research on Cancer suggested arsenic as a class-1 carcinogen. The underlying mechanism pertaining to arsenic-induced carcinogenesis is still enigmatic. Although plentiful evidences have vouched that the redox machinery is the main culprit for arsenic-induced carcinogenesis, however several reports have documented regarding participation of mitochondria as the root originators of the redox signaling in arsenic-induced carcinogenesis. Moreover, the redox machinery system plays a vital role in regulating mitochondrial biogenesis and homeostasis. However, there is still a knowledge gap regarding the influence of redox machinery systems on mitochondrial biogenesis and homeostasis in the development of arsenic-induced carcinogenesis. The objectives of this paper are to review and evaluate the role of mitochondrial biogenesis in the development of arsenic-induced carcinogenesis in addition to the possible therapeutic option for modulation of such signaling mechanisms.

Mitochondrial biogenesis alteration in arsenic-induced carcinogenesis and its therapeutic interventions