Review of chromium (VI) apoptosis, cell-cycle-arrest, and carcinogenesis

A. Chiu, X. L. Shi, W. K. P. Lee, R. Hill, T. P. Wakeman, A. Katz, B. Xu, N. S. Dalal, J. D. Robertson, C. Chen, N. Chiu, L. Donehower

Research output: Contribution to journalArticlepeer-review


Hexavalent chromium combines with glutathione in chloride intracellular channel carrier to form tetravalent and pentavalent chromium in plasma and organelle membranes. It also combines with NADH/NADPH to form pentavalent chromium in mitochondria. Tetravalent- and pentavalent- chromium (directly and indirectly) mediated DNA double strand breaks activate DNA damage signaling sensors: DNA-dependent-protein-kinase signals p53-dependent intrinsic mitochondrial apoptosis, and ataxia-telangiectasia-mutated and ataxia-telangiectasia-Rad3-related signal cell-arrest for DNA repair. Tetravalent chromium may be the most potent species since it causes DNA breaks and somatic recombination, but not apoptosis. Upon further failure of apoptosis and senescence/DNA-repair, damaged cells may become immortal with loss-of-heterozygosity and genetic plasticity.
Original languageEnglish
Pages (from-to)188-230
Number of pages43
JournalJournal of Environmental Science and Health, Part A
Issue number3
Publication statusPublished - 31 Aug 2010
Externally publishedYes


  • chloride intracellular channel carrier
  • tetravalent chromium
  • pentavalent chromium
  • apoptosis
  • senescence
  • somatic recombination
  • genomic plasticity


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