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j. Soc. Cosmet. Chem., 41, 187-195 (May/June 1990) Chronic ultraviolet radiation-induced skin tumors and associated changes in basal epidermal ornithine decarboxylase activity GREGG. HILLEBRAND, MARCIA S. WINSLOW, DAVE A. HEITMEYER, and DONALD L. BISSETT, The Procter & Gamble Company, Miami Valley Laboratories, Cincinnati, OH 45239-8707. Received April 13, 1990. Synopsis The association between ultraviolet radiation (UVR)-induced skin neoplasia and the basal levels of the epidermal enzyme ornithine decarboxylase (ODC) was studied in Skh:HR-1 hairless mice. Groups of mice were chronically exposed to UVR (15 weeks), then treated with photoprotective agents (12-20 weeks) with or without continued UVR exposure. After treatment, total skin papilloma/carcinoma (tumor) area per mouse and epidermal ODC activity (in the treated and UVR-exposed but non-tumor-involved dorsal skin) were measured in each group. Mice with the largest average tumor area had substantially elevated basal ODC activities (•350-fold) relative to non-irradiated control mice, which lacked tumors. Groups of mice treated with photoprotective agents showed intermediate levels of skin tumors and correspondingly inter- mediate epidermal ODC activities. Basal epidermal ODC activity was also measured in lifetime sun-exposed and unexposed skin of four healthy human volunteers with no history of skin cancer. No significant relationship was observed between human epidermal ODC activity and prior history of solar exposure in these individuals. These human data are consistent with recent hairless mouse studies [Hillebrand, G. G., Winslow, M. S., Benzinger, M. A., Heirmeyer, D. A., and Bissett, D. L., Cancer Res., 50, 1580-1584 (1990)] showing that chronically irradiated mice lacking visible tumors had normal levels of epidermal ODC activity. The results support the idea that elevated levels of epidermal ODC activity may be specifically indicative of chronic UVR-in- duced neoplastic growth. INTRODUCTION The visible appearance of skin, especially facial skin, can be very dependent on an individual's past history of solar radiation exposure. For example, chronic solar radia- tion exposure can lead to damage of the underlying dermal connective tissue (1-4), manifested as accelerated visible skin aging in the form of wrinkles (5-8). In more severe cases, chronic photodamage can progress to the most common forms of skin cancer, i.e., basal and squamous cell carcinoma (9). The diagnosis and development of therapy for photodamaged skin is facilitated by the employment of biochemical markers 187