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

doi:10.1080/10590501.2010.504980

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

Toxicology and Cancer Biology

Research output: Contribution to journal › Review article › peer-review

94 Scopus citations

Abstract

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 language	English
Pages (from-to)	188-230
Number of pages	43
Journal	Journal of Environmental Science and Health - Part C Environmental Carcinogenesis and Ecotoxicology Reviews
Volume	28
Issue number	3
DOIs	https://doi.org/10.1080/10590501.2010.504980
State	Published - Jul 2010

Bibliographical note

Funding Information:
All the authors with to acknowledge the support of their respective institutions. Dr. Xianglin Shi wishes especially to acknowledge the generous support of NIH grant 1R01CA116697.

Keywords

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

ASJC Scopus subject areas

Health, Toxicology and Mutagenesis
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1080/10590501.2010.504980

Cite this

Chiu, A., Shi, X. L., Lee, W. K. P., Hill, R., Wakeman, T. P., Katz, A., Xu, B., Dalal, N. S., Robertson, J. D., Chen, C., Chiu, N., & Donehower, L. (2010). Review of chromium (VI) apoptosis, cell-cycle-arrest, and carcinogenesis. Journal of Environmental Science and Health - Part C Environmental Carcinogenesis and Ecotoxicology Reviews, 28(3), 188-230. https://doi.org/10.1080/10590501.2010.504980

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abstract = "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.",

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Chiu, A, Shi, XL, Lee, WKP, Hill, R, Wakeman, TP, Katz, A, Xu, B, Dalal, NS, Robertson, JD, Chen, C, Chiu, N & Donehower, L 2010, 'Review of chromium (VI) apoptosis, cell-cycle-arrest, and carcinogenesis', Journal of Environmental Science and Health - Part C Environmental Carcinogenesis and Ecotoxicology Reviews, vol. 28, no. 3, pp. 188-230. https://doi.org/10.1080/10590501.2010.504980

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AU - Shi, X. L.

AU - Lee, W. K.P.

AU - Hill, R.

AU - Wakeman, T. P.

AU - Katz, A.

AU - Xu, B.

AU - Dalal, N. S.

AU - Robertson, J. D.

AU - Chen, C.

AU - Chiu, N.

AU - Donehower, L.

N1 - Funding Information: All the authors with to acknowledge the support of their respective institutions. Dr. Xianglin Shi wishes especially to acknowledge the generous support of NIH grant 1R01CA116697.

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N2 - 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.

AB - 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.

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

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

UN SDGs

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