ULTRAVIOLET-B RADIATION-INDUCED DNA LESIONS IN MOUSE EPIDERMIS - AN ASSESSMENT USING A NOVEL P-32 POSTLABELING TECHNIQUE

Ultraviolet B (UVB) component of the sunlight is the major cause of no nmelanoma skin cancer (NMSC) in humans. UVB is absorbed directly by ce llular DNA and produces lesions that may cause mutation(s) in target g ene(s) ultimately leading to cancer. Early detection of these lesions, therefore, may help to identify individuals at a high risk to develop NMSC, and devise approaches for the prevention of this common maligna ncy. Employing mouse skin as a model, we applied a P-32 postlabelling, method to detect UVB-induced DNA lesions in the epidermis in nanomole quantities. Autoradiography maps showed that epidermal DNA from UVB e xposed mice al 24 h contain up to five DNA lesions; the quantitation o f these lesions showed that their formation increased in a WE dose-dep endent manner. Treatment of DNA samples with the bacteriophage DNA rep air enzyme T4 endonuclease V confirmed that four of these lesions are pyrimidine dimers. While, some of these lesions were repaired 18 h aft er WE irradiation, 30% of them persisted even 48 h post-irradiation. A pplication of a sunscreen containing ethylhexyl-p-methoxycinnamate or chemopreventive agent green tea polyphenols or silymarin to the skin o f the mice prior to UVB exposure was found to prevent the formation of pyrimidine dimers. (C) 1996 Academic Press, Inc.