Ultraviolet-induced dna repair synthesis in lymphocytes from patients with actinic keratosis.
Actinic keratosis is an epidermal cancer in situ. Extensive exposure to sunlight is considered as a contributing factor to the etiology of this tumor. Ultraviolet (UV) light of solar radiation induces structural damage in DNA, which may give rise to mutations and transformed cells if the damage is not repaired. Repair of UV-induced DNA lesions is an essential property of human cells. The conditions so far reported to have defective DNA repair are all associated with an increased incidence of malignancy. Do patients with actinic keratosis also exhibit a reduced capacity to repair UV-induced DNA lesions? DNA repair synthesis in peripheral leukocytes was studied in 10 patients with actinic keratosis and 10 healthy subjects of corresponding age. After irradiation with various doses of UV light the leukocytes were incubated for 2 hr with [3H]thymidine in the presence of hydroxyurea. A dose-response relationship for the UV-induced DNA repair synthesis was established for each individual. The average repair capacity in the patients with actinic keratosis was about 30% below that of the controls. The difference is statistically significant (p less than 0.02). Reduced DNA repair synthesis may therefore be an important factor in the etiology of actinic keratosis.
D000368:Aged; D002986:Clinical Trials as Topic; D004260:DNA Repair / Q000528:radiation effects*; D004261:DNA Replication / Q000187:drug effects; D004307:Dose-Response Relationship, Radiation; D005260:Female; D006801:Humans; D006918:Hydroxyurea / Q000494:pharmacology; D007642:Keratosis / Q000209:etiology / Q000378:metabolism*; D008214:Lymphocytes / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D011230:Precancerous Conditions / Q000378:metabolism*; D012878:Skin Neoplasms / Q000378:metabolism*; D014466:Ultraviolet Rays
D006918:Hydroxyurea