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Carcinogenesis, Vol. 23, No. 4, 605-609, April 2002
© 2002 Oxford University Press

CARCINOGENESIS

Demonstration of UV-dimers in human skin DNA in situ 3 weeks after exposure

Kari Hemminki1,3, Guogang Xu1, Laura Kause2, Leena M. Koulu2, Chunyan Zhao1 and Christer T. Jansen2

1 Department of Biosciences at Novum, Karolinska Institute, 14157 Huddinge, Sweden and
2 Department of Dermatology, University of Turku, 20520 Turku, Finland

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.


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