ArticleChemical research in toxicology2010
Mechanism of DNA-protein cross-linking by chromium.
Article in Chemical research in toxicology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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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Who cites it
32 citing papers in PubMed, 84 citations in OpenAlex.
- Cr(VI) and DON co-exposure triggers intestinal epithelial cells ferroptosis and pyroptosis through Nrf2/NF-κB/NLRP3 to impair intestinal barrier function.Redox report : communications in free radical research · 2026Article
- Isotope Dilution NanoLC-MS/MS Quantitation of Methylglyoxal DNA-Protein Cross-Links: Formation and Repair in Human Cells.Analytical chemistry · 2026Article
- Isotope Dilution nanoLC-MS/MS Quantitation of Methylglyoxal DNA-Protein Crosslinks: Formation and Repair in Human Cells.bioRxiv : the preprint server for biology · 2025Article
- ATR activation by Cr-DNA damage is a major survival response establishing late S and G2 checkpoints after Cr(VI) exposure.Toxicology and applied pharmacology · 2023Article
- Chemical mechanisms of DNA damage by carcinogenic chromium(VI).Advances in pharmacology (San Diego, Calif.) · 2023Article
- Influence of heavy metals in Parkinson's disease: an overview.Journal of neurology · 2022Review
- Hexavalent chromium disrupts chromatin architecture.Seminars in cancer biology · 2021Review
- Toxic Mechanisms of Five Heavy Metals: Mercury, Lead, Chromium, Cadmium, and Arsenic.Frontiers in pharmacology · 2021Review
- DNA-protein crosslinks from environmental exposure: Mechanisms of formation and repair.Environmental and molecular mutagenesis · 2020Review
- Safety and efficacy of AvailaEFSA journal. European Food Safety Authority · 2020Article
- Mechanisms of Chromium-Induced Toxicity.Current opinion in toxicology · 2019Article
- Toxicological Antagonism among Welding Fume Metals: Inactivation of Soluble Cr(VI) by Iron.Chemical research in toxicology · 2018Article
- Variation in Extracellular Detoxification Is a Link to Different Carcinogenicity among Chromates in Rodent and Human Lungs.Chemical research in toxicology · 2017Article
- Carcinogenicity of chromium and chemoprevention: a brief update.OncoTargets and therapy · 2017Review
- Myricetin induces apoptosis via endoplasmic reticulum stress and DNA double-strand breaks in human ovarian cancer cells.Molecular medicine reports · 2016Article
- Different ATM Signaling in Response to Chromium(VI) Metabolism via Ascorbate and Nonascorbate Reduction: Implications for in Vitro Models and Toxicogenomics.Environmental health perspectives · 2016Article
- Proteasome activity is important for replication recovery, CHK1 phosphorylation and prevention of G2 arrest after low-dose formaldehyde.Toxicology and applied pharmacology · 2015Article
- DNA-Protein Cross-Links: Formation, Structural Identities, and Biological Outcomes.Accounts of chemical research · 2015Article
- Review
- DNA double-strand breaks by Cr(VI) are targeted to euchromatin and cause ATR-dependent phosphorylation of histone H2AX and its ubiquitination.Toxicological sciences : an official journal of the Society of Toxicology · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Hexavalent chromium is a known inducer of DNA-protein cross-links (DPCs) that contribute to repression of inducible genes and genotoxicity of this metal. Lymphocytic DPCs have also shown potential utility as biomarkers of human exposure to Cr(VI). Here, we examined the mechanism of DPC formation by Cr(VI) and the impact of its main cellular reducers. In vitro reactions of Cr(VI) with one-electron reducing thiols (glutathione and cysteine) or two-electron donating ascorbate were all efficient at DPC production, indicating a dispensable role of Cr(V). No Cr(VI) reducer was able to generate DPC in the presence of Cr(III)-chelating EDTA or phosphate. A critical role of Cr(III) in DNA-protein linkages was further confirmed by dissociation of Cr(VI)-induced DPC by phosphate. EDTA was very inefficient in DPC dissociation, indicating its poor suitability for testing of Cr(III)-mediated bridging and reversal of complex DPC. Reactions containing only one Cr-modified component (protein or DNA) showed that Cr(III)-DNA adduction was the initial step in DPC formation. Cross-linking proceeded slowly after the rapid formation of Cr-DNA adducts, indicating that protein conjugation was the rate-limiting step in DPC generation. Experiments with depletion of glutathione and restoration of ascorbate levels in human lung A549 cells showed that high cellular reducing capacity promotes DPC yield. Overall, our data provide evidence for a three-step cross-linking mechanism involving (i) reduction of Cr(VI) to Cr(III), (ii) Cr(III)-DNA binding, and (iii) protein capture by DNA-bound Cr(III) generating protein-Cr(III)-DNA cross-links.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.