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Mutagenesis Advance Access originally published online on April 13, 2006
Mutagenesis 2006 21(3):205-211; doi:10.1093/mutage/gel016
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© The Author 2006. Published by Oxford University Press. All rights reserved.
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org

Possible involvement of XPA in repair of oxidative DNA damage deduced from analysis of damage, repair and genotype in a human population study

Mária Dusinská1,*, Zuzana Dzupinková1, Ladislava Wsólová1, Vikki Harrington2 and Andrew R. Collins2,3

1 Department of Experimental and Applied Medicine, Institute of Preventive and Clinical Medicine, Research Base of Slovak Medical University Limbová 14, 83303 Bratislava, Slovakia 2 School of Life Sciences, Robert Gordon University Aberdeen, UK 3 Department of Nutrition, University of Oslo Oslo, Norway

Participants in a study of occupational exposure to mineral fibres in Slovakia were analysed for the polymorphism 23A->G in the DNA repair gene XPA. Of the 388 subjects, 239 were exposed to asbestos, stonewool or glass fibre; the rest were unexposed controls. Levels of DNA base alterations (oxidation and alkylation) in lymphocytes were measured using the comet assay with lesion-specific endonucleases. 8-oxoguanine DNA glycosylase (OGG1) DNA repair activity was measured, as incision activity of a lymphocyte extract on DNA containing the OGG1 substrate 8-oxoguanine. Presence of the A allele was associated with higher levels of DNA damage (sites sensitive to formamidopyrimidine DNA glycosylase, endonuclease III or 3-methyladenine DNA glycosylase II) as well as with higher activity of OGG1 repair enzyme. DNA base damage increased with age, showing highly significant correlations when the whole population or subgroups of the population were analysed. OGG1 repair activity also increased with age, but when analysed according to XPA genotype, the increase was observed only in those individuals with an A allele. Although XPA is known as a protein involved in nucleotide excision repair of UV-induced damage and bulky DNA adducts, it may also have a role in the repair of oxidized bases.

*To whom correspondence should be addressed. Tel: +421259369270; Fax: +421259369270; Email: maria.dusinska{at}szu.sk


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