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Carcinogenesis Advance Access originally published online on January 16, 2004
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Carcinogenesis, Vol. 25, No. 5, 757-763, May 2004
Carcinogenesis vol.25 no.5 © Oxford University Press 2004; all rights reserved.

ARTICLE

Genetic polymorphisms in DNA repair genes and possible links with DNA repair rates, chromosomal aberrations and single-strand breaks in DNA

Pavel Vodicka1,11, Rajiv Kumar2,3, Rudolf Stetina4, Somali Sanyal2, Pavel Soucek5, Vincent Haufroid6, Maria Dusinska7, Miroslava Kuricova7, Maria Zamecnikova8, Ludovit Musak9, Jana Buchancova9, Hannu Norppa10, Ari Hirvonen10, Ludmila Vodickova5, Alessio Naccarati1, Zora Matousu1 and Kari Hemminki2,3

1 Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Videnska 1083, 14200 Prague 4, Czech Republic, 2 Department of Bioscience at Novum, Karolinska Institute, Huddinge, Sweden, 3 German Cancer Institute, Heidelberg, Germany, 4 Purkynje Military Medical Academy, Hradec Kralove, Czech Republic, 5 National Institute of Public Health, Prague, Czech Republic, 6 Catholic University of Louvain, Louvain, Belgium, 7 Institute of Preventive and Clinical Medicine, Bratislava, Slovak Republic, 8 National Institute of Public Health, Bratislava, Slovak Republic, 9 Department of Occupational Medicine, Medical Faculty in Martin, Martin, Slovak Republic and 10 Finnish Institute of Occupational Health, Helsinki, Finland

11 To whom correspondence should be addressed. Tel: +420 2 241062694; Email: pvodicka{at}biomed.cas.cz

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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