Carcinogenesis Advance Access published online on October 6, 2006
Carcinogenesis, doi:10.1093/carcin/bgl187
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1 Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic
* To whom correspondence should be addressed. We investigated association between polymorphisms in DNA repair genes and the capacity to repair DNA damage induced by
Received June 22, 2006
Revised September 25, 2006
Accepted September 27, 2006
MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION
Association of DNA repair polymorphisms with DNA repair functional outcomes in healthy human subjects
Pavel Vodicka 1 *, Rudolf Stetina 2, Veronika Polakova 1, Elena Tulupova 1, Alessio Naccarati 1, Ludmila Vodickova 3, Rajiv Kumar 4, Monika Hanova 1, Barbara Pardini 5, Jana Slyskova 1, Ludovit Musak 6, Giuseppe De Palma 7, Pavel Soucek 8, and Kari Hemminki 4
2 Purkynje Military Medical Academy, Hradec Kralove, Czech Republic
3 Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic; Center of Occupational Medicine, National Institute of Public Health, Prague, Czech Republic
4 Division of Molecular Genetic Epidemiology, German Cancer Research Center, Heidelberg, Germany; Department of Biosciences at Novum, Karolinska Institute, Huddinge, Sweden
5 Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic; Department of Biology, University of Pisa, Italy
6 Department of Medical Biology, Jessenius Medical Faculty, Comenius Univesity Martin, Slovak Republic
7 Laboratory of Industrial Toxicology, Department of Clinical Medicine, Nephrology and Health Sciences, University of Parma, Italy
8 Center of Occupational Medicine, National Institute of Public Health, Prague, Czech Republic
Pavel Vodicka, E-mail: pvodicka{at}biomed.cas.cz
Abstract 
-irradiation and by base oxidation in a healthy population. Irradiation-specific DNA repair rates were significantly decreased in individuals with XRCC1 Arg399Gln homozygous variant genotype (0.45±0.47 SSB/109 daltons) than in those with wild-type genotype (1.10±0.70 SSB/109 daltons, P=0.0006, Mann-Witney U-test). The capacity to repair oxidative DNA damage was significantly decreased among individuals with hOGG1 Ser326Cys homozygous variant genotype (0.37±0.28 SSB/109 daltons) compared to those with wild-type genotype (0.83±0.79 SSB/109 daltons, P=0.008, Mann-Witney U-test). Investigation of genotype combinations showed that the increasing number of variant alleles for both XRCC1 Arg399Gln and APE1 Asn148Glu polymorphisms resulted in a significant decrease of irradiation-specific repair rates (P=0.008, Kruskal-Wallis test). Irradiation-specific DNA repair rates also decreased with increasing number of variant alleles in XRCC1 Arg399Gln in combination with variant alleles for two other XRCC1 polymorphisms, Arg194Trp and Arg280His, P=0.002 and P=0.005, respectively; Kruskal-Wallis test). In a binary combination variant alleles of hOGG1 Ser326Cys and APE1 Asn148Glu polymorphisms were associated with a significant decrease in the capacity to repair DNA oxidative damage (P=0.018, Kruskal-Wallis test). In summary, XRCC1 Arg399Gln and hOGG1 Ser326Cys polymorphisms seem to exert the predominant modulating effect on irradiation-specific DNA repair capacity and the capacity to repair DNA oxidative damage, respectively.
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