ArticleJournal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS)2012
Metabolism of Cr(VI) by ascorbate but not glutathione is a low oxidant-generating process.
Article in Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 18 citations in OpenAlex.
- Carcinogenic Mechanisms of Hexavalent Chromium: From DNA Breaks to Chromosome Instability and Neoplastic Transformation.Current environmental health reports · 2024Review
- Chemical mechanisms of DNA damage by carcinogenic chromium(VI).Advances in pharmacology (San Diego, Calif.) · 2023Article
- A comparison of particulate hexavalent chromium cytotoxicity and genotoxicity in human and leatherback sea turtle lung cells from a one environmental health perspective.Toxicology and applied pharmacology · 2019Article
- Review
- Chromium(VI) causes interstrand DNA cross-linking in vitro but shows no hypersensitivity in cross-link repair-deficient human cells.Chemical research in toxicology · 2013Article
- Mechanistic insights from the NTP studies of chromium.Toxicologic pathology · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Genotoxic activity of hexavalent chromium (chromate) results from its reductive activation inside the cell. Cr(VI) metabolism in vivo is primarily driven by ascorbate (Asc) but in cultured cells by glutathione (GSH). Given the common use of cultured cells for mechanistic studies, it is important to establish whether Cr(VI) activated by Asc and GSH displays the same genotoxic properties. Using 2',7' dichlorofluorescin (DCFH) as a redox sensitive probe, we found that Asc-dependent reduction of Cr(VI) in vitro under physiological conditions generated 25-80 times lower yields of oxidants compared to GSH. When both reducers were present, Asc dominated Cr(VI) metabolism and inhibited DCFH oxidation. Consistent with the findings in defined chemical reactions, restoration of physiological levels of Asc in human lung H460 cells led to the loss of their hypersensitivity to clonogenic killing by Cr(VI) in the presence of methoxyamine, which inhibits base excision repair of oxidative DNA damage. Despite suppressed oxidative damage, Asc-containing cells formed a large number of DNA double-strand breaks after exposure to a dose of Cr(VI) corresponding to the drinking water standard of 100 ppb. Our results indicate that Asc-driven metabolism of Cr(VI) shifts its genotoxicity toward nonoxidative mechanisms.
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