A pooled analysis of molecular epidemiological studies on modulation of DNA repair by host factors
Language English Country Netherlands Media print-electronic
Document type Journal Article
PubMed
35483778
DOI
10.1016/j.mrgentox.2022.503447
PII: S1383-5718(22)00008-0
Knihovny.cz E-resources
- Keywords
- BMI, Base excision repair, Biomarker, Comet assay, DNA repair, Oxidatively damaged DNA,
- MeSH
- DNA-Formamidopyrimidine Glycosylase MeSH
- Epidemiologic Studies MeSH
- Comet Assay MeSH
- Middle Aged MeSH
- Humans MeSH
- DNA Repair * genetics MeSH
- DNA Damage * MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- DNA-Formamidopyrimidine Glycosylase MeSH
Levels of DNA damage represent the dynamics between damage formation and removal. Therefore, to better interpret human biomonitoring studies with DNA damage endpoints, an individual's ability to recognize and properly remove DNA damage should be characterized. Relatively few studies have included DNA repair as a biomarker and therefore, assembling and analyzing a pooled database of studies with data on base excision repair (BER) was one of the goals of hCOMET (EU-COST CA15132). A group of approximately 1911 individuals, was gathered from 8 laboratories which run population studies with the comet-based in vitro DNA repair assay. BER incision activity data were normalized and subsequently correlated with various host factors. BER was found to be significantly higher in women. Although it is generally accepted that age is inversely related to DNA repair, no overall effect of age was found, but sex differences were most pronounced in the oldest quartile (>61 years). No effect of smoking or occupational exposures was found. A body mass index (BMI) above 25 kg/m2 was related to higher levels of BER. However, when BMI exceeded 35 kg/m2, repair incision activity was significantly lower. Finally, higher BER incision activity was related to lower levels of DNA damage detected by the comet assay in combination with formamidopyrimidine DNA glycosylase (Fpg), which is in line with the fact that oxidatively damaged DNA is repaired by BER. These data indicate that BER plays a role in modulating the steady-state level of DNA damage that is detected in molecular epidemiological studies and should therefore be considered as a parallel endpoint in future studies.
Department of Biology Faculty of Medicine Slovak Medical University 833 03 Bratislava Slovakia
Department of Non ionizing Radiation National Public Health Center H 1221 Budapest Hungary
Department of Nutrition University of Oslo Norway
Gazi University Faculty of Pharmacy Department of Toxicology Etiler Ankara 06330 Turkey
Mutagenesis Unit Institute for Medical Research and Occupational Health Zagreb Croatia
Oslo Metropolitan University Faculty of Health Sciences PO Box 4 St Olavs plass 0130 Oslo Norway
References provided by Crossref.org
A pooled analysis of host factors that affect nucleotide excision repair in humans