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Cited by 200Arsenic contamination and mitigationCarcinogens and Genotoxicity AssessmentHeavy Metal Exposure and Toxicity

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Arsenic Exposure Is Associated with Decreased DNA Repair in Vitro and in Individuals Exposed to Drinking Water Arsenic

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Andrew, Angeline S., Burgess, Jefferey L., Meza, Maria M., Demidenko, Eugene, Waugh, Mary G., Hamilton, Joshua W., Karagas, Margaret R.·2006·Environmental Health Perspectives
DOI 10.1289/ehp.9008PMC PMC1552016
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Abstract

The mechanism(s) by which arsenic exposure contributes to human cancer risk is unknown; however, several indirect cocarcinogenesis mechanisms have been proposed. Many studies support the role of As in altering one or more DNA repair processes. In the present study we used individual-level exposure data and biologic samples to investigate the effects of As exposure on nucleotide excision repair in two study populations, focusing on the excision repair cross-complement 1 (ERCC1) component. We measured drinking water, urinary, or toenail As levels and obtained cryopreserved lymphocytes of a subset of individuals enrolled in epidemiologic studies in New Hampshire (USA) and Sonora (Mexico). Additionally, in corroborative laboratory studies, we examined the effects of As on DNA repair in a cultured human cell model. Arsenic exposure was associated with decreased expression of ERCC1 in isolated lymphocytes at the mRNA and protein levels. In addition, lymphocytes from As-exposed individuals showed higher levels of DNA damage, as measured by a comet assay, both at baseline and after a 2-acetoxyacetylaminofluorene (2-AAAF) challenge. In support of the in vivo data, As exposure decreased ERCC1 mRNA expression and enhanced levels of DNA damage after a 2-AAAF challenge in cell culture. These data provide further evidence to support the ability of As to inhibit the DNA repair machinery, which is likely to enhance the genotoxicity and mutagenicity of other directly genotoxic compounds, as part of a cocarcinogenic mechanism of action.

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  • AsIII affects zinc fingers by binding with its target molecule PARP-1, leading to single-strand and double-strand DNA breaks and oxidative DNA damage.

    “Zhou et al. [106] reported that AsIII affects zinc fingers by binding with its target molecule PARP-1, ultimately leading to breaks of single-strand and double-strand of DNA and oxidative DNA damage [107].”

    From Arsenic Contamination of Groundwater: A Review of Sources, Prevalence, Health Risks, and Strategies for Mitigation (2014) · cites this paper as [107]

    The Discussion reports that arsenic exposure inhibits DNA repair and can exacerbate damage caused by other mutagens. It does not establish that arsenic causes single- and double-strand breaks or oxidative DNA damage; it says direct DNA damage from inorganic arsenic is controversial. In the citing sentence, the PARP-1 and zinc-finger mechanism is attributed to Zhou et al. [106], not to this source [107]. (LLM, conf=0.83)

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References 45 · Cited by 200

Research works printed but not linked: 37

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Metadata

Authors
Andrew, A. S., Burgess, J. L., Meza, M. M., Demidenko, E., Waugh, M. G., Hamilton, J. W., & Karagas, M. R.
Affiliations
  • Dartmouth College (US)
  • University of Arizona (US)
  • Department of Natural Resources, Technological Institute of Sonora (ITSON), Ciudad Obregon, Sonora, Mexico
Corresponding author
Andrew, Angeline S.
ORCID
Venue
Environmental Health Perspectives
Publisher
American Chemical Society (ACS)
Published
2006-05-10
Volume
114
Issue
8
Pages
1193-1198
ISSN
  • 0091-6765 (ISSN-L)
  • 1552-9924
DOI
10.1289/ehp.9008
PMC
PMC1552016
OpenAlex
W2060866949
Cited by
200
References
45
Citations by year
2026: 6 · 2025: 3 · 2024: 4 · 2023: 5 · 2022: 5 · 2021: 10 · 2020: 3 · 2019: 7 · 2018: 11 · 2017: 7 · 2016: 11 · 2015: 17 · 2014: 19 · 2013: 14 · 2012: 9
FWCI
13.51
Type
journal article
Language
en
Open access
Licence
Locations
  • Environmental Health Perspectives (publishedVersion, public-domain)
  • PubMed (publishedVersion)
Funders
  • Dartmouth College
  • American Society of Preventive Oncology
  • National Institutes of Health (RR018787, ES 06694, ES-00002, 5p20rr018787-07)
  • National Cancer Institute (CA82354, R01CA082354, CA 57494, R01CA057494, CA099500, R03CA099500)
  • National Institute of Environmental Health Sciences (ES05947, P42ES007373, ES-07373, ES 06694, P42ES005947, P30ES000002, ES 00002, P30ES006694)
  • National Center for Research Resources (RR 018787, P20-RR018787)
Topics
  • Physical Sciences › Environmental Science › Environmental Chemistry › Arsenic contamination and mitigation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Heavy Metal Exposure and Toxicity
Keywords
arsenic exposure, DNA repair, nucleotide excision repair, ERCC1, drinking water arsenic, lymphocytes, DNA damage, cocarcinogenesis, genotoxicity, urinary arsenic, toenail arsenic, comet assay, cancer risk
MeSH terms
Adult, Arsenic, DNA Damage, DNA Repair, DNA-Binding Proteins, Electrophoresis, Polyacrylamide Gel, Endonucleases, Environmental Exposure, Female, Genetic Markers, Humans, Male, Mexico, Middle Aged, Nails, New Hampshire, RNA, Water Supply, Blotting, Western, Gene Expression, Reverse Transcriptase Polymerase Chain Reaction, Comet Assay

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