ReviewEnvironmental health perspectives2002
Oxidative DNA adducts and DNA-protein cross-links are the major DNA lesions induced by arsenite.
Review in Environmental health perspectives, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 107 citations in OpenAlex.
- Hsp70 is phosphorylated in a conserved response to DNA damage and contributes to cell cycle control.eLife · 2026Article
- Arsenome, Arsenobolome, and Arsenobiolome.International journal of molecular sciences · 2025Review
- A conserved Hsp70 phosphorylation regulates cell cycle progression after DNA damage.bioRxiv : the preprint server for biology · 2025Article
- Urothelial genotoxicity of household chemicals in healthy canine urinary bladder organoids relative to observed urinary exposures in pet dogs.Frontiers in veterinary science · 2025Article
- Nano‑zinc enhances gene regulation of non‑specific immunity and antioxidative status to mitigate multiple stresses in fish.Scientific reports · 2023Article
- Arsenic and cancer: Evidence and mechanisms.Advances in pharmacology (San Diego, Calif.) · 2023Article
- Tetraspanin CD9: A friend or foe of head and neck cancer (Review).Oncology reports · 2022Review
- Melatonin: a pleiotropic hormone as a novel potent therapeutic candidate in arsenic toxicity.Molecular biology reports · 2021Review
- Investigating the impact of long term exposure to chemical agents on the chromosomal radiosensitivity using human lymphoblastoid GM1899A cells.Scientific reports · 2021Article
- DNA-protein crosslinks from environmental exposure: Mechanisms of formation and repair.Environmental and molecular mutagenesis · 2020Review
- Molecular Mechanisms of Arsenic-Induced Disruption of DNA Repair.Chemical research in toxicology · 2020Review
- A review of arsenic exposure and lung cancer.Toxicology research · 2019Review
- Roles ofJournal of bacteriology · 2019Article
- Sulforaphane potentially attenuates arsenic-induced nephrotoxicity via the PI3K/Akt/Nrf2 pathway in albino Wistar rats.Environmental science and pollution research international · 2019Article
- Redox balance and DNA fragmentation in arsenic-exposed occupational workers from different industries of Pakistan.Environmental science and pollution research international · 2018Article
- Molecular insight of arsenic-induced carcinogenesis and its prevention.Naunyn-Schmiedeberg's archives of pharmacology · 2017Review
- Bypass of DNA-Protein Cross-links Conjugated to the 7-Deazaguanine Position of DNA by Translesion Synthesis Polymerases.The Journal of biological chemistry · 2016Article
- An Overview of Carcinogenic Heavy Metal: Molecular Toxicity Mechanism and Prevention.Journal of cancer prevention · 2015Review
- Arsenic Disruption of DNA Damage Responses-Potential Role in Carcinogenesis and Chemotherapy.Biomolecules · 2015Review
- Error-prone translesion synthesis past DNA-peptide cross-links conjugated to the major groove of DNA via C5 of thymidine.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Arsenic is recognized to be a nonmutagenic carcinogen because it induces DNA damage only at very high concentrations. However, many more DNA strand breaks could be detected by digesting the DNA of arsenite-treated cells with endonuclease III, formamidopyrimidine-DNA glycosylase, and proteinase K. By doing so, arsenite could be shown to induce DNA damage in human cells within a pathologically meaningful concentration range. Oxidized guanine products were detected in all arsenite-treated human cells examined. DNA-protein cross-links were also detected in arsenite-treated NB4 and HL60 cells. In human umbilical vein endothelial cells, the induction of oxidized guanine products by arsenite was sensitive to inhibitors of nitric oxide (NO) synthase but not to oxidant modulators, whereas the opposite result was obtained in vascular smooth muscle cells. On the other hand, the arsenite-induced oxidized guanine products and DNA-protein cross-links in NB4 and HL60 cells were sensitive to modulators of calcium, NO synthase, oxidant, and myeloperoxidase. Therefore, although oxidized guanine products were detected in all the human cells treated with arsenite, the pathways could be different in different cell types. Because the sensitivity and the mechanism of arsenic intoxication are cell specific, it is important that target tissues and target cells are used for investigations. It is also important that pathologically or pharmacologically meaningful concentrations of arsenic are used. This is because in most cases we are dealing with the chronic effect rather than acute toxicity.
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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.