Journal Article

Demonstration of UV-dimers in human skin DNA <i>in situ</i> 3 weeks after exposure

Kari Hemminki, Guogang Xu, Laura Kause, Leena M. Koulu, Chunyan Zhao and Christer T. Jansen

in Carcinogenesis

Volume 23, issue 4, pages 605-609
Published in print April 2002 | ISSN: 0143-3334
Published online April 2002 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/23.4.605
Demonstration of UV-dimers in human skin DNA in situ 3 weeks after exposure

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Data on DNA repair rates of specific types of DNA lesions are very limited in humans in situ. Rate of repair of UV-induced DNA damage was followed in the skin of 17 volunteers up to 3 weeks of UV exposure, using a 32P-postlabelling technique for the determination of specific photoproducts. The subjects of skin phototypes I and IV were exposed to 40 mJ/cm2 of solar simulating radiation on buttock skin, and biopsies were taken at 0 h, 48 h and 3 weeks of exposure for the analysis of two cyclobutane pyrimidine dimers, TT=C and TT=T, and two 6-4 photoproducts, TT-C and TT-T, as trinucleotides. Repair rates were heterogeneous for different photoproducts. T=T dimers were repaired slower than C=T dimers, and 2.3–9.0% of the initial T=T damage remained unrepaired after 3 weeks, and was detectable in 16/17 subjects. The identity of the identified photoproducts was confirmed by a photochemical reversion assay. Damage level correlated with skin types, type I being more sensitive than type IV in an age-matched comparison. This is the first time the persistence of defined human DNA damage is demonstrated up to 3 weeks. Long-lasting DNA damage increases the likelihood of mutations.

Keywords: CPD, cyclobutane pyrimidine dimers; TT=C and TT=T, cyclobutane dimers; SSR, solar simulating radiation; MED, minimal erythemal dose; NER, nucleotide excision repair.

Journal Article.  4138 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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