Molecular and Cellular Biochemistry

, Volume 255, Issue 1, pp 57–66

Molecular mechanisms of arsenic carcinogenesis

Authors

  • Chuanshu Huang
    • Nelson Institute of Environmental Medicine, New York University School of Medicine
  • Qingdong Ke
    • Nelson Institute of Environmental Medicine, New York University School of Medicine
  • Max Costa
    • Nelson Institute of Environmental Medicine, New York University School of Medicine
  • Xianglin Shi
    • Health Effects Laboratory Division, National Institute for Occupational Safety and Health
Article

DOI: 10.1023/B:MCBI.0000007261.04684.78

Cite this article as:
Huang, C., Ke, Q., Costa, M. et al. Mol Cell Biochem (2004) 255: 57. 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.

arseniccarcinogenesisgene expressinreactive oxygen speciesgenetic toxicitysignal transductionkinasemethylation
Download to read the full article text

Copyright information

© Kluwer Academic Publishers 2004