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

Liu, Cheng; Liu, Shaojun; Dixon, Kathleen

doi:10.2307/3434147

Cited by 16 publications

(17 citation statements)

References 10 publications

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“…However, Cr treatment does enhance 8-oxoG formation, possibly as a result of diminished Ogg1p activity (Hodges & Chipman, 2002), but just not at a level that causes Cr toxicity according to our results. Similarly, although Cr(VI) causes alternative oxidative lesions to DNA that are repairable by Apn1p in S. cerevisiae (Cheng et al, 1998), even in a quadruple apn1/rad1/ntg1/ntg2 mutant, such lesions were not sufficient to elicit a Cr(VI) hypersensitivity phenotype (O'Brien et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Oxidative protein damage causes chromium toxicity in yeast

et al. 2005

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Oxidative damage in microbial cells occurs during exposure to the toxic metal chromium, but it is not certain whether such oxidation accounts for the toxicity of Cr. Here, a Saccharomyces cerevisiae sod1D mutant (defective for the Cu,Zn-superoxide dismutase) was found to be hypersensitive to Cr(VI) toxicity under aerobic conditions, but this phenotype was suppressed under anaerobic conditions. Studies with cells expressing a Sod1p variant (Sod1 H46C ) showed that the superoxide dismutase activity rather than the metal-binding function of Sod1p was required for Cr resistance. To help identify the macromolecular target(s) of Cr-dependent oxidative damage, cells deficient for the reduction of phospholipid hydroperoxides (gpx3D and gpx1D/gpx2D/gpx3D) and for the repair of DNA oxidation (ogg1D and rad30D/ogg1D) were tested, but were found not to be Cr-sensitive. In contrast, S. cerevisiae msraD (mxr1D) and msrbD (ycl033cD) mutants defective for peptide methionine sulfoxide reductase (MSR) activity exhibited a Cr sensitivity phenotype, and cells overexpressing these enzymes were Cr-resistant. Overexpression of MSRs also suppressed the Cr sensitivity of sod1D cells. The inference that protein oxidation is a primary mechanism of Cr toxicity was corroborated by an observed~20-fold increase in the cellular levels of protein carbonyls within 30 min of Cr exposure. Carbonylation was not distributed evenly among the expressed proteins of the cells; certain glycolytic enzymes and heat-shock proteins were specifically targeted by Cr-dependent oxidative damage. This study establishes an oxidative mode of Cr toxicity in S. cerevisiae, which primarily involves oxidative damage to cellular proteins.

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Section: Discussionmentioning

confidence: 99%

Oxidative protein damage causes chromium toxicity in yeast

et al. 2005

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“…Compared to the recommended permissible limit of 2 mg/L prescribed by BIS, India alone released about 2000-3000 tons of chromium into the environment annually from tanneries with chromium concentrations ranging between 40-5000mg/L. Chromium is a potential pollutant and well known for its mutagenicity (Cheng and Dixon, 1998) and carcinogenicity (Wang et al, 1999) effects in humans, animals and plants. Soil profile, surface water bodies (ponds and rivers), human health, fishes and other aquatic biodiversities are at risk of serious threat due to the extensive use of chromium in tanning industries and discharge of wastewater (Mohanta et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Assessment of Physico-Chemical Properties of Tannery Waste Water and Its Impact on Fresh Water Quality

Bharose¹,

Singh²

2017

Int.J.Curr.Microbiol.App.Sci

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“…Researchers are using shuttle vector systems in yeast, mammalian cells, and lung tissue of transgenic mice to investigate the mechanisms of chromate mutagenesis (66,67). Chromate is reduced by glutathione, and mutagenesis is influenced by tissue levels of glutathione.…”

Section: Combustion By-products: Concerns and Current Researchmentioning

confidence: 99%

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

Cited by 16 publications

References 10 publications

Oxidative protein damage causes chromium toxicity in yeast

Oxidative protein damage causes chromium toxicity in yeast

Assessment of Physico-Chemical Properties of Tannery Waste Water and Its Impact on Fresh Water Quality

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

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