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

Role of mitochondria, ROS, and DNA damage in arsenic induced carcinogenesis. Front Biosci (Schol Ed). 2016 Jun 01;8:312-20 Authors: Lee CH, Yu HS Abstract 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. PMID: 27100709 [PubMed - indexed for MEDLINE]
Source: Frontiers in Bioscience - Scholar - Category: Biomedical Science Tags: Front Biosci (Schol Ed) Source Type: research