HAIR DAMAGE PREVENTION BY COCONUT OIL 339 REFERENCES (1) M.L. Garcia and J. Diaz, Combability measurements on human hair, J. Soc. Cosmet. Chem., 27, 379-398 (1976). (2) L.J. Wolfram, J. Soc. Cosmet. Chem., 21,875 (1970). (3) S.S. Sandhu and C. Robbins, A simple and sensitive technique, based on protein loss measurement, to assess surface damage to human hair, J. Soc. Cosmet. Chem., 44, 163-175 (1993). (4) J. A. Swift and A. C. Brown, The critical determination of fine changes in the surface architecture of human hair due to cosmetic treatments. J. Soc. Cosmet. Chem., 23, 695-702 (1972). (5) J. A. Swift, Int. J. Cosmet. Sci., 13, 143 (1991). (6) S. B. Ruetsch and H. D. Weigmann, J. Soc. Cosmet. Chem., 47, 13-26 (1996).
j. Cosmet. sci., 50, 341-349 (November/December 1999) DNA damaoe, repair, and tannino acceleration A. A. VINK, P. T. M. VAN DEN BERG, and L. ROZA, TNO Nutrition and Food Research Institute, Skin EfjScts Testing and Photobiology, P.O. Box 360, 3700 AJ Zeist, The Netherlands Accepted jSr publication October 15, 1999. Synopsis Exposure of the skin to solar ultraviolet radiation (UV) leads to various adverse effects, such as the induction of cellular damage and mutations, suppression of the skin's immune system, and the induction of skin cancer. These effects are the consequence of various molecular alterations in the skin resulting from absorption of photons. Formation of DNA damage is one of these. In the present study the effect of tanning accelerators was investigated on the level of DNA damage after exposure to UV. With the use of a specific monoclonal antibody, DNA damage was quantified in human skin. Epicutaneous application of a complex of tanning enhancers (Unipertan © VEG-2002) before exposure to UV was found to reduce the level of DNA damage at 6 and/or 24 h thereafter. The results of in vitro studies (human skin organ cultures) as well as of a preliminary clinical trial are presented. The tanning enhancer was shown to increase removal of UV-DNA damage over normal repair measured at 6 and 24 h after UV exposure. INTRODUCTION Exposure of man to ultraviolet radiation (UV) is increasing due to changes in life style: sun holidays and the use of artificial tanning equipment have gained popularity, and a well-tanned skin is often considered a sign of good health. In addition, the depletion of stratospheric ozone may result in an increase in short-wavelength UV (UVB) reaching the earth's surface. The most serious harmful effect of UV for humans is the formation of malignant cells in the skin: mutated cells resulting from UV-infiicted DNA damage may be given the opportunity, during a state of UV-induced immunosuppression, to grow unimpeded and progress into a tumor (1-3). Solar ultraviolet light is divided into two subregions: a short-wavelength region, UVB (290-315 nm), and a long-wavelength region, UVA (315-400 nm). Nucleic acids like DNA strongly absorb the radiant energy from UVB especially. The ensuing excitations of electrons result in chemical modification of DNA. Among the different types of DNA damage formed upon UVB irradiation, cyclobutane pyrimidine dimers (CPD) are pre- dominant (Figure 1). The possible biological consequences of DNA damage are mani- fold. During cell replication a faulty base may be built into the new DNA strand opposite a modified base. This mutation may lead to altered expression of genes that play a central role in growth, differentiation, and carcinogenesis. In addition, CPD have been shown to play a role in the suppression of immune responses after UVB exposure (4). 341
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