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

Producción científica: Review article › revisión exhaustiva

100 Citas (Scopus)

Resumen

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.

Idioma original	English
Páginas (desde-hasta)	188-230
Número de páginas	43
Publicación	Journal of Environmental Science and Health - Part C Environmental Carcinogenesis and Ecotoxicology Reviews
Volumen	28
N.º	3
DOI	https://doi.org/10.1080/10590501.2010.504980
Estado	Published - jul 2010

Nota bibliográfica

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.

Financiación

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.

Financiadores	Número del financiador
National Institutes of Health (NIH)
National Childhood Cancer Registry – National Cancer Institute	R01CA116697

ASJC Scopus subject areas

Health, Toxicology and Mutagenesis
Cancer Research

ODS de las Naciones Unidas

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10.1080/10590501.2010.504980

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

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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author = "A. Chiu and Shi, \{X. L.\} and Lee, \{W. K.P.\} and R. Hill and Wakeman, \{T. P.\} and A. Katz and B. Xu and Dalal, \{N. S.\} and Robertson, \{J. D.\} and C. Chen and N. Chiu and L. Donehower",

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.",

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doi = "10.1080/10590501.2010.504980",

language = "English",

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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, n.º 3, pp. 188-230. https://doi.org/10.1080/10590501.2010.504980

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AU - Chiu, A.

AU - Shi, X. L.

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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

Resumen

Nota bibliográfica

Financiación

ASJC Scopus subject areas

ODS de las Naciones Unidas

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