A pooled analysis of molecular epidemiological studies on modulation of DNA repair by host factors
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378041%3A_____%2F22%3A00568752" target="_blank" >RIV/68378041:_____/22:00568752 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/00216208:11110/22:10444938 RIV/00216208:11140/22:10444938
Výsledek na webu
<a href="https://www.sciencedirect.com/science/article/abs/pii/S1383571822000080?via%3Dihub" target="_blank" >https://www.sciencedirect.com/science/article/abs/pii/S1383571822000080?via%3Dihub</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1016/j.mrgentox.2022.503447" target="_blank" >10.1016/j.mrgentox.2022.503447</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
A pooled analysis of molecular epidemiological studies on modulation of DNA repair by host factors
Popis výsledku v původním jazyce
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 hCOME T (EU-COST CA15132). A group of approximately 1911 individuals, was gathered from 8 laboratories which r u n 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 overal l effect of age was found, but se x 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/m(2) was related to higher levels of BER. However, when BMI exceeded 35 kg/m(2), 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.
Název v anglickém jazyce
A pooled analysis of molecular epidemiological studies on modulation of DNA repair by host factors
Popis výsledku anglicky
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 hCOME T (EU-COST CA15132). A group of approximately 1911 individuals, was gathered from 8 laboratories which r u n 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 overal l effect of age was found, but se x 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/m(2) was related to higher levels of BER. However, when BMI exceeded 35 kg/m(2), 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.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
10601 - Cell biology
Návaznosti výsledku
Projekt
—
Návaznosti
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2022
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Mutation Research - Genetic Toxicology and Environmental Mutagenesis
ISSN
1383-5718
e-ISSN
1879-3592
Svazek periodika
876
Číslo periodika v rámci svazku
feb.
Stát vydavatele periodika
NL - Nizozemsko
Počet stran výsledku
7
Strana od-do
503447
Kód UT WoS článku
000793346500010
EID výsledku v databázi Scopus
2-s2.0-85123800711