348 JOURNAL OF COSMETIC SCIENCE has been suggested (7-9). Enhancement of DNA repair, by delivery of repair enzymes to UV-damaged skin cells or cultured melanocytes, was shown to increase UV-induced melanin synthesis. Moreover, application of repair products (e.g., small DNA frag- ments), thereby mimicking DNA repair, was shown to induce tanning in unexposed skin via the upregulation of mRNA for tyrosinase. It was concluded that one of the signals initiating UV-induced melanogenesis is the excision of DNA photoproducts. It can be hypothesized that both pathways, melanogenesis and the DNA repair process, share one or more mediators. The objective of the present study was to investigate whether this relationship between DNA repair and tanning is also true the other way around, whether stimulatoin of melanin synthesis results in enhancement of DNA repair. In order to activate melano- genesis and to induce DNA photoproducts, human skin was exposed to UVB that had been epicutaneously treated with tanning enhanceres (Unipertan © VEG-2002). This complex contains several precursors of melanin and, when applied to skin before UV exposure, has been shown to increase tanning significantly (6). As expected, 1-h incu- bation of the skin with Unipertan © VEG-2002 followed by a single dose of UV did not result in protection against formation of DNA damage. For tanning to be induced, providing a natural sunscreen, more time and preferably multiple exposures are required. A stimulatory effect was found on DNA damage removal, both in vitro in cultured skin (three donors) and in vivo (two out of three volunteers). The effect observed on photo- product repair may indicate that one or more, as yet unknown, mediators shared by the tanning response and the repair pathway have been activated by the tanning accelerators. Alternatively, one or more of the ingredients of Unipertan © VEG-2002 may have positively affected the repair process. CONCLUSIONS The present study indicates that tanning enhancers (Unipertan © VEG-2002) may pro- vide photoprotection in two ways: (a) UV-induced melanogenesis is enhanced, providing a natural sunscreen, and melanin effectively absorbs UV, preventing further induction of cellular damage (b) removal of DNA damage, which has been shown to contribute to UV-induced mutagenesis, immunosuppression, and skin cancer, is enhanced. ACKNOWLEDGMENT We acknowledge the support of the studies by Uni-Chemie AG (subsidiary of Induchem Holding AG, Switzerland). REFERENCES (1) D. E. Brash, J. A. Rudolph, J. A. Simon, A. Lin, G. J. McKenna, H. P. Baden, A. J. Halperin, and J. Ponten, A role for sunlight in skin cancer: UV-induced p53 mutations in squamous cell carcinoma, Proc. Nat/. Acad. Sci. USA, 88, 10124-10128 (1991). (2) M. L. Kripke and M. S. Fisher, Immunologic parameters of ultraviolet carcinogenesis,J. Nat/. Cancer Inst., 57, 211-215 (1976).
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