The DOI matches its Crossref record; 169 of the 179 references it cites were found in a registry or an index.
Mutagenicity and repair of oxidative DNA damage: insights from studies using defined lesions
Abstract
Vinyl chloride monomer (VCM) is a human carcinogen. However, the exact mechanism of carcinogenesis remains unclear. VCM may be metabolized by cytochrome P450 2E1 (CYP2E1), aldehyde dehydrogenase 2 (ALDH2) and glutathione S-transferases (GSTs). Thus workers with inherited variant metabolic enzyme activities may have an altered risk of genotoxicity. This study was designed to investigate which risk factors might affect sister chromatid exchange (SCE) frequency in polyvinyl chloride (PVC) workers. Study subjects were 44 male workers from three PVC factories. Questionnaires were administered to obtain detailed histories of cigarette smoking, alcohol consumption, occupations, and medications. SCE frequency in peripheral lymphocytes was determined using a standardized method, and CYP2E1, GSTM1, GSTT1 and ALDH2 genotypes were identified by the polymerase chain reaction (PCR). Analysis revealed that smoking status and exposure to VCM were significantly associated with increased SCE frequency. The presence of ALDH2 1-2/2-2 genotypes was also significantly associated with an elevation of SCE frequency (9. 5 vs. 8.1, p<0.01). However, CYP2E1, GSTM1 or GSTT1 genotypes were not significantly associated with SCE frequency. When various genotypes were considered together, combination of CYP2E1 c1c2/c2c2 with ALDH2 1-2/2-2 showed an additive effect on SCE frequency. Similar results were also found for the combination of smoking with CYP2E1, or smoking with ALDH2. These results suggest that VCM workers with ALDH2 1-2/2-2 genotypes, who also smoke, may have increased risk of DNA damage.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“The most common oxidative lesions in mtDNA are the G:C to T:A transversion mutations caused by adenine pairing with the guanine adduct 7,8-dihydro-8-oxo-deoxyguanosine (8-oxo-dG) (Wang et al., 1998).”
From Role of the mitochondrial DNA replication machinery in mitochondrial DNA mutagenesis, aging and age-related diseases (2017) · cites this paper as Wang et al., 1998
Citations
Cites
1 retracted
Cooper, P. K., Nouspikel, T. P., Clarkson, S. G., & Leadon, S. A. (1997) · Science · doi:10.1126/science.275.5302.990 · Cited by 306
RetractedFree radicals in biology and medicine
Gutteridge, J. M. C. (1991) · General Pharmacology The Vascular System · doi:10.1016/0306-3623(91)90478-o · Cited by 17,178
Oxidants, antioxidants, and the degenerative diseases of aging.
Ames, B. N., Shigenaga, M. K., & Hagen, T. M. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.17.7915 · Cited by 5,958
Friedberg, E. C., Walker, G. C., Siede, W., Wood, R. D., Schultz, R. A., & Ellenberger, T. (2005) · doi:10.1128/9781555816704 · Cited by 5,683
Free Radicals in Biology and Medicine
Land, E. J. (1990) · International Journal of Radiation Biology · doi:10.1080/09553009014552071 · Cited by 4,871
Bootsma, D., & Hoeijmakers, J. H. J. (1996) · Trends in Genetics · doi:10.1016/0168-9525(96)81408-9 · Cited by 2,285
Insertion of specific bases during DNA synthesis past the oxidation-damaged base 8-oxodG
Shibutani, S., Takeshita, M., & Grollman, A. P. (1991) · Nature · doi:10.1038/349431a0 · Cited by 2,224
The Chemical Basis of Radiation Biology
O'Neill, P. (1987) · International Journal of Radiation Biology and Related Studies in Physics Chemistry and Medicine · doi:10.1080/09553008714552571 · Cited by 1,849
8-Hydroxyguanine, an abundant form of oxidative DNA damage, causes G-T and A-C substitutions.
Cheng, K. C., Cahill, D. S., Kasai, H., Nishimura, S., & Loeb, L. A. (1992) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)48474-8 · Cited by 1,844
The chemical basis of radiation biology
von Sonntag, C. (1987) · Medical Entomology and Zoology · Cited by 1,748
Cited by
Sorted by citations
Marnett, L. J. (2000) · Carcinogenesis · doi:10.1093/carcin/21.3.361 · Cited by 1,922
Role of oxygen radicals in DNA damage and cancer incidence
Valko, M., Izakovic, M., Mazur, M., Rhodes, C. J., & Telser, J. (2004) · Molecular and Cellular Biochemistry · doi:10.1023/b:mcbi.0000049134.69131.89 · Cited by 1,820
Hussain, S. P., Hofseth, L. J., & Harris, C. C. (2003) · Nature Reviews Cancer · doi:10.1038/nrc1046 · Cited by 1,690
The Role of Oxidative Stress in Carcinogenesis
Klaunig, J. E., & Kamendulis, L. M. (2004) · The Annual Review of Pharmacology and Toxicology · doi:10.1146/annurev.pharmtox.44.101802.121851 · Cited by 1,568
Halliwell, B. (2001) · Drugs & Aging · doi:10.2165/00002512-200118090-00004 · Cited by 1,502
Metadata
- Authors
- Wang, D., Kreutzer, D. A., & Essigmann, J. M.
- Affiliations
- Massachusetts Institute of Technology (US)
- Corresponding author
- Essigmann, John M.
- Venue
- Mutation research. Fundamental and molecular mechanisms of mutagenesis
- Publisher
- Elsevier BV
- Published
- 1998-05
- Volume
- 400
- Issue
- 1-2
- Pages
- 99-115
- ISSN
- 0027-5107 (ISSN-L)
- 1386-1964
- OpenAlex
- W2009187135
- Cited by
- 464
- References
- 179
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 5 · 2023: 5 · 2022: 8 · 2021: 8 · 2020: 9 · 2019: 11 · 2018: 10 · 2017: 15 · 2016: 14 · 2015: 19 · 2014: 21 · 2013: 21 · 2012: 22
- FWCI
- 6.41
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Mutation research. Fundamental and molecular mechanisms of mutagenesis (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA and Nucleic Acid Chemistry
- Keywords
- oxidative DNA damage, mutagenicity, DNA repair, reactive oxygen species, mutational spectra, G:C to T:A transversions, G:C to A:T transitions, DNA adducts, mutational specificity, carcinogenesis, aging
- MeSH terms
- Animals, DNA Damage, DNA Mutational Analysis, DNA Repair, Humans, Oxidation-Reduction, Mutagenesis, Site-Directed, Reactive Oxygen Species, DNA Adducts
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
