IMR Press / FBS / Volume 8 / Issue 2 / DOI: 10.2741/S465

Frontiers in Bioscience-Scholar (FBS) is published by IMR Press from Volume 13 Issue 1 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.


Role of mitochondria, ROS, and DNA damage in arsenic induced carcinogenesis

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1 Department of Dermatology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan
2 Department of Dermatology, Kaohsiung Medical University, Kaohsiung, Taiwan
3 National Environmental Research Center, National Health Research Institutes, Zhunan, Taiwan

*Author to whom correspondence should be addressed.

Academic Editors: Yau-Huei Wei, Myung-Shik Lee

Front. Biosci. (Schol Ed) 2016, 8(2), 312–320;
Published: 1 June 2016

The International Agency for Research on Cancer (IARC) declared arsenic a class I carcinogen. Arsenic exposure induces several forms of human cancers, including cancers of skin, lung, liver, and urinary bladder. The majority of the arsenic-induced cancers occur in skin. Among these, the most common is Bowen’s disease, characterized by epidermal hyperplasia, full layer epidermal dysplasia, leading to intraepidermal carcinoma as well as apoptosis, and moderate dermal infiltrates, which require the participation of mitochondria. The exact mechanism underlying arsenic induced carcinogenesis remains unclear, although increased reactive oxidative stresses, leading to chromosome abnormalities and uncontrolled growth, and aberrant immune regulations might be involved. Here, we highlight how increased mitochondrial biogenesis and oxidative stress lead to mitochondrial DNA damage and mutation in arsenic induced cancers. We also provide therapeutic rationale for targeting mitochondria in the treatment of arsenic induced cancers.

DNA Damages
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