Signaling by carcinogenic metals and metal-induced reactive oxygen species

Mutat Res. 2003 Dec 10;533(1-2):183-200. doi: 10.1016/j.mrfmmm.2003.08.025.


Epidemiological data indicate that exposure to metal and metalloid species, including arsenic(III), chromium(VI), and nickel(II), increases the risk of cancer, particularly of the lung and skin. Alterations in normal signal transduction as a result of exposure to carcinogenic metals, and to metal-catalyzed reactive oxygen species (ROS) formation, appear to play an important role in the etiology of metal-induced carcinogenesis. Signaling components affected by metals include growth factor receptors, G-proteins, MAP kinases, and nuclear transcription factors. This article reviews current literature on the effects of carcinogenic metals and metal-induced ROS on cancer-related signaling pathways. In addition, the mechanisms by which those changes occur, and the role of those changes in carcinogenesis are discussed.

Publication types

  • Review

MeSH terms

  • Animals
  • Carcinogens / toxicity*
  • Humans
  • Metals / toxicity*
  • Neoplasms / chemically induced
  • Neoplasms / metabolism
  • Rats
  • Reactive Oxygen Species / toxicity*
  • Signal Transduction / drug effects*


  • Carcinogens
  • Metals
  • Reactive Oxygen Species