Molecular mechanisms of arsenic carcinogenesis

Mol Cell Biochem. 2004 Jan;255(1-2):57-66. doi: 10.1023/b:mcbi.0000007261.04684.78.

Abstract

Arsenic is a metalloid compound that is widely distributed in the environment. Human exposure of this compound has been associated with increased cancer incidence. Although the exact mechanisms remain to be investigated, numerous carcinogenic pathways have been proposed. Potential carcinogenic actions for arsenic include oxidative stress, genotoxic damage, DNA repair inhibition, epigenetic events, and activation of certain signal transduction pathways leading to abberrant gene expression. In this article, we summarize current knowledge on the molecular mechanisms of arsenic carcinogenesis with an emphasis on ROS and signal transduction pathways.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Arsenic / metabolism
  • Arsenic / toxicity*
  • Cell Transformation, Neoplastic / chemically induced*
  • Cricetinae
  • Cytokines / metabolism
  • DNA Damage / physiology
  • DNA Repair / physiology
  • Environmental Pollutants / adverse effects*
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • Mice
  • Mutagens / metabolism
  • Oncogenes / physiology
  • Oxidative Stress / physiology
  • Protein Kinases / metabolism
  • Rabbits
  • Rats
  • Reactive Oxygen Species / metabolism*
  • Signal Transduction / drug effects*
  • Transcription Factors / metabolism

Substances

  • Cytokines
  • Environmental Pollutants
  • Mutagens
  • Reactive Oxygen Species
  • Transcription Factors
  • Protein Kinases
  • Arsenic