Arsenic Exposure and the Induction of Human Cancers

Figure 2

Schematic representation of proposed arsenic-induced carcinogenic mechanisms. Arsenic can enter cells in both tri- or pentavalent forms (As^III or As^V). Inside cells, As^V is converted to As^III, with subsequent methylation to monomethylated (MMA) and dimethylated (DMA) species. The methylation of inorganic arsenic consumes both S-adenosylmethionine (SAM) and glutathione (GSH). Cellular damage derived from arsenic biotransformation can occur through generation of reactive oxygen species (ROS), and through epigenetic mechanisms: changes in DNA methylation patterns (by depletion of cellular pools of methyl group), histone modification, and altered expression of microRNAs (miRNAs).