Signaling by carcinogenic metals and metal-induced reactive oxygen species

Gabriel Keith Harris, Xianglin Shi

Research output: Contribution to journalReview articlepeer-review

139 Scopus citations


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.

Original languageEnglish
Pages (from-to)183-200
Number of pages18
JournalMutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
Issue number1-2
StatePublished - Dec 10 2003


  • Metals
  • Reactive oxygen species
  • Signal transduction

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Health, Toxicology and Mutagenesis


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