Induction of mutagenic DNA damage by chromium(VI) and glutathione

Liu, Shaojun; Dixon, Kathleen

doi:10.1002/(sici)1098-2280(1996)28:2<71::aid-em2>3.0.co;2-h

Cited by 45 publications

(22 citation statements)

References 42 publications

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“…Chromate and its derivatives have been shown to cause Cr-DNA adducts and DNA-DNA cross-links (11,27,28,43,47,53,59,64,65), which can disrupt regulation of gene expression or change DNA topology, leading to altered cell function and perhaps even cell death. Cr(III) can cause DNA damage and negatively affect DNA topology by directly inhibiting topoisomerase DNA relaxation activity (40).…”

Section: Vol 72 2006mentioning

confidence: 99%

“…Cr(VI)-induced apoptosis, for example, was demonstrated in p53 human bronchoalveolar cells (46), and Cr(VI) exposure results in a spectrum of genomic damage in cultured cells including DNA single-strand and double-strand breaks, binding of amino acids and proteins to DNA, DNA interstrand crosslinks, and Cr-DNA adducts (11,27,28,43,47,53,59,64,65). Cr toxicity is also associated with the generation of reactive oxygen intermediates during the intracellular partial reduction of Cr(VI) to the unstable intermediate Cr(V) by various in vivo nonspecific reductants (e.g., glutathione, NADH, NADPH, and cysteine) or cellular one-electron reductases (16,27,50). The other most stable, common form of chromium, trivalent Cr(III), is considered less toxic than Cr(VI) because of its tendency to form insoluble hydrated Cr 3ϩ complexes, which cannot cross cell membranes.…”

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confidence: 98%

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Global Molecular and Morphological Effects of 24-Hour Chromium(VI) Exposure on Shewanella oneidensis MR-1

Chourey

Thompson

Morrell‐Falvey

et al. 2006

Appl Environ Microbiol

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The biological impact of 24-h ("chronic") chromium(VI) [Cr(VI) or chromate] exposure on Shewanella oneidensis MR-1 was assessed by analyzing cellular morphology as well as genome-wide differential gene and protein expression profiles. Cells challenged aerobically with an initial chromate concentration of 0.3 mM in complex growth medium were compared to untreated control cells grown in the absence of chromate. At the 24-h time point at which cells were harvested for transcriptome and proteome analyses, no residual Cr(VI) was detected in the culture supernatant, thus suggesting the complete uptake and/or reduction of this metal by cells. In contrast to the untreated control cells, Cr(VI)-exposed cells formed apparently aseptate, nonmotile filaments that tended to aggregate. Transcriptome profiling and mass spectrometry-based proteomic characterization revealed that the principal molecular response to 24-h Cr(VI) exposure was the induction of prophage-related genes and their encoded products as well as a number of functionally undefined hypothetical genes that were located within the integrated phage regions of the MR-1 genome. In addition, genes with annotated functions in DNA metabolism, cell division, biosynthesis and degradation of the murein (peptidoglycan) sacculus, membrane response, and general environmental stress protection were upregulated, while genes encoding chemotaxis, motility, and transport/binding proteins were largely repressed under conditions of 24-h chromate treatment.The metal oxyanion chromate (CrO 4 2Ϫ ) is a widespread environmental contaminant due to its prevalent use in industrial and defense applications such as tanning, electroplating, paint pigment manufacturing, stainless steel welding, and nuclear weapons production (25,26). The hexavalent form of chromium, Cr(VI), is highly soluble and toxic, with chronic exposure leading to mutagenesis and carcinogenesis. Cr(VI)-induced apoptosis, for example, was demonstrated in p53 human bronchoalveolar cells (46), and Cr(VI) exposure results in a spectrum of genomic damage in cultured cells including DNA single-strand and double-strand breaks, binding of amino acids and proteins to DNA, DNA interstrand crosslinks, and Cr-DNA adducts (11,27,28,43,47,53,59,64,65). Cr toxicity is also associated with the generation of reactive oxygen intermediates during the intracellular partial reduction of Cr(VI) to the unstable intermediate Cr(V) by various in vivo nonspecific reductants (e.g., glutathione, NADH, NADPH, and cysteine) or cellular one-electron reductases (16,27,50). The other most stable, common form of chromium, trivalent Cr(III), is considered less toxic than Cr(VI) because of its tendency to form insoluble hydrated Cr 3ϩ complexes, which cannot cross cell membranes. However, Cr(III) was shown to cause DNA damage and inhibit topoisomerase DNA relaxation activity in bacteria (40).The adverse biological impact of Cr(VI) is attributable to the cellular uptake process. Chromate is transported across eukaryotic and prokaryotic cellular membranes vi...

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Section: Vol 72 2006mentioning

confidence: 99%

mentioning

confidence: 98%

Global Molecular and Morphological Effects of 24-Hour Chromium(VI) Exposure on Shewanella oneidensis MR-1

Chourey

Thompson

Morrell‐Falvey

et al. 2006

Appl Environ Microbiol

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“…We have used shuttle vectors in yeast (24) and mammalian systems (25,26) and the Big Blue transgenic mouse system (27) The C57BL/6 Big Blue transgenic mouse carries the bacterial lad gene in a bacteriophage X-based vector integrated into the mouse chromosome (32). For chromium treatment, mice (4-to 6-week-old females) were anesthetized, and a small surgical cut was made in the ventral neck to expose the trachea; a chromium solution was injected with a 30.5-gauge needle through the wall of the trachea into the lungs.…”

Section: Introductionmentioning

confidence: 98%

Analysis of Repair and Mutagenesis of Chromium-Induced DNA Damage in Yeast, Mammalian Cells, and Transgenic Mice

Liu¹,

Liu²,

Dixon³

1998

Environmental Health Perspectives

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“…Compounds of Cr(VI), but not Cr(III), have been found to be mutagenic and carcinogenic (64). Chromate (CrO 4 2-), the major ionic form of Cr(VI), readily penetrates cell membranes (65).…”

Section: Combustion By-products: Concerns and Current Researchmentioning

confidence: 75%

The origin, fate, and health effects of combustion by-products: a research framework.

Avakian

Dellinger

Fiedler

et al. 2002

Environ Health Perspect

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Incomplete combustion processes can emit organic pollutants, metals, and fine particles. Combustion by-products represent global human and environmental health challenges that are relevant not only in heavily industrialized nations, but also in developing nations where up to 90% of rural households rely on unprocessed biomass fuels for cooking, warmth, and light. These issues were addressed at the Seventh International Congress on Combustion By-Products, which convened 4-6 June 2001 in Research Triangle Park, North Carolina. This congress included a diverse group of multidisciplinary researchers and practitioners who discussed recent developments and future goals in the control of combustion by-products and their effects of exposure on human and ecologic health. Participants recommended that interdisciplinary, coordinated research efforts should be focused to capitalize on the important potential synergisms between efforts to reduce the adverse human health effects linked to exposures to combustion by-products and broader efforts to reduce greenhouse gas emissions and save energy through efficiency. In this article we summarize the principal findings and recommendations for research focus and direction.

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Induction of mutagenic DNA damage by chromium(VI) and glutathione

Cited by 45 publications

References 42 publications

Global Molecular and Morphological Effects of 24-Hour Chromium(VI) Exposure on Shewanella oneidensis MR-1

Global Molecular and Morphological Effects of 24-Hour Chromium(VI) Exposure on Shewanella oneidensis MR-1

Analysis of Repair and Mutagenesis of Chromium-Induced DNA Damage in Yeast, Mammalian Cells, and Transgenic Mice

The origin, fate, and health effects of combustion by-products: a research framework.

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