Genetic polymorphisms in DNA repair genes and possible links with DNA repair rates, chromosomal aberrations and single-strand breaks in DNA
Language English Country Great Britain, England Media print-electronic
Document type Journal Article, Multicenter Study, Research Support, Non-U.S. Gov't
PubMed
14729591
DOI
10.1093/carcin/bgh064
PII: bgh064
Knihovny.cz E-resources
- MeSH
- Chromosome Aberrations * MeSH
- DNA-Binding Proteins genetics MeSH
- DNA Helicases * MeSH
- Adult MeSH
- Endonucleases MeSH
- Exons genetics MeSH
- Nuclear Proteins MeSH
- DNA, Single-Stranded genetics MeSH
- Codon MeSH
- Humans MeSH
- DNA Repair genetics MeSH
- Polymorphism, Genetic * MeSH
- DNA Damage genetics MeSH
- X-ray Repair Cross Complementing Protein 1 MeSH
- Proteins genetics MeSH
- Mutagenicity Tests MeSH
- Transcription Factors * MeSH
- Xeroderma Pigmentosum Group D Protein MeSH
- Check Tag
- Adult MeSH
- Humans MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Multicenter Study MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- DNA excision repair protein ERCC-5 MeSH Browser
- DNA-Binding Proteins MeSH
- DNA Helicases * MeSH
- Endonucleases MeSH
- ERCC2 protein, human MeSH Browser
- Nuclear Proteins MeSH
- DNA, Single-Stranded MeSH
- Codon MeSH
- X-ray Repair Cross Complementing Protein 1 MeSH
- Proteins MeSH
- Transcription Factors * MeSH
- X-ray repair cross complementing protein 3 MeSH Browser
- Xeroderma Pigmentosum Group D Protein MeSH
- XPC protein, human MeSH Browser
- XRCC1 protein, human MeSH Browser
We analysed the associations between genetic polymorphisms in genes coding for DNA repair enzymes XPD (exon 23 A --> C, K751Q), XPG (exon 15 G --> C, D1104H), XPC (exon 15 A --> C, K939Q), XRCC1 (exon 10 G --> A, R399Q) and XRCC3 (exon 7 C --> T, T241 M) and the levels of chromosomal aberrations (CAs) and single-strand breaks (SSBs) in peripheral lymphocytes in a central European population. We also measured the irradiation-specific DNA repair rates and the repair rates of 8-oxoguanines in these individuals. An elevated frequency of CAs was observed in individuals with the XPD exon 23 A allele (AA and AC) genotypes (F = 3.6, P = 0.028, ANOVA). In multifactorial analysis of variance, the XPD exon 23 polymorphism appeared as a major factor influencing CAs (F = 4.2, P = 0.017). SSBs in DNA, on the other hand, were modulated by XPD (F = 4.3, P = 0.023), XPG (F = 4.3, P = 0.024) and XRCC1 genotypes (F = 3.0, P = 0.064). Irradiation-specific DNA repair rates (reflecting mainly base excision repair activity) were affected by XRCC1 (F = 5.9, P = 0.010) and XPC polymorphisms (F = 4.2, P = 0.046, MANOVA). Our results from this study suggest that markers of genotoxicity are associated with polymorphisms in genes encoding DNA repair enzymes.
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