Molecular mechanisms of Cr(VI)-induced carcinogenesis

Min Ding, Xianglin Shi

Research output: Contribution to journalArticlepeer-review

114 Scopus citations

Abstract

Although Cr(VI)-containing compounds are well documented carcinogens, their mechanism of action is still not well understood. Recent studies have suggested that reduction of Cr(VI) to its lower oxidation states and related free radical reactions play an important role in Cr(VI)-induced carcinogenesis. This article summarizes recent studies from our laboratory on (a) the reduction of Cr(VI) by ascorbate, diol- and thiol-containing molecules, certain flavoenzymes, cell organelles, intact cells, and whole animals; (b) free radical production in both non-cellular and cellular systems; and (c) Cr(VI)-induced DNA damage, activation of nuclear transcription factor κB (NF-κB), activator protein-1, p53, hypoxia-inducible factor-1, vascular endothelial growth factor, tyrosine phosphorylation, apoptosis, cell growth arrest, and gene expression profile.

Original languageEnglish
Pages (from-to)293-300
Number of pages8
JournalMolecular and Cellular Biochemistry
Volume234-235
DOIs
StatePublished - 2002

Keywords

  • Apoptosis
  • Carcinogenesis
  • Cell growth arrest
  • Cr(VI)
  • Reactive oxygen species
  • Signal transduction
  • Transcriptional regulation

ASJC Scopus subject areas

  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

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