UV light is considered an important contributor to skin cancer, but methods have been lacking to quantify specific UV-induced lesions in human skin in situ. We applied a newly developed 32P-postlabeling technique to measure specific UV-induced cyclobutane dimers and 6-4 dipyrimidine lesions in the skin of healthy volunteers. At a dose of 400 J/m2, solar-simulated radiation caused at least 20 cyclobutane dimers/10(6) nucleotides, which is much higher than any known DNA adducts induced by specific external chemical exposure in human target tissues. This may explain why patients with DNA repair syndromes, such as xeroderma pigmentosum, preferentially develop skin cancer. We applied the 32P-postlabeling technique to study rates of DNA repair in healthy individuals. The obtained data indicated a base sequence dependence of the repair process. The applied method has potential for the study of DNA repair as a determinant of individual susceptibility to skin cancer.

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