346 JOURNAL OF COSMETIC SCIENCE lOO 90 80 70 60 50 40 30 l lO o A donor 1 donor 2 donor 3 100 90 80 70 60 50 40 30 20 10 0 donor 1 I donor 2 donor 3 Figure 4. CPD reduction measured at 6 h (A) and 24 h (B) after irradiation of human skin organ cultures from three donors. Treatments: 3000 J/m 2 UVB (black bar) and Unipertan © VEG-2002 followed by 3000 J/m = UVB (hatched bar). representative of the data obtained with human volunteers, and therefore the human skin organ culture appears to be a suitable model for photobiology studies (b) variation exists in the reduction of DNA damage levels when comparing skin from different individuals, ranging from no to almost complete reduction of CPD within 24 h after exposure. When the level of DNA damage found at 24 h is reduced to what is measured immediately

DNA DAMAGE AND REPAIR 347 lOO 9o 80 70 60 50 40 30 20 lO o I I volunteer I volunteer 2 volunteer 3 Figure 5. CPD reduction measured at 24 h after ix vivo irradiation of skin from three volunteers. Treat- ments: 3 MED UVB (black bar) and Unipertan © VEG-2002 followed by 3 MED UVB (hatched bar). after exposure, this reduction is very likely to be the result of the skin's repair system. Alternatively, one should take into account the theoretical possibility that within this time period the photoproduct has not actually been repaired but it merely no longer detectable. In the present discussion we prefer to refer to the term "repair" when dimer levels are reduced. The observation of absence of repair in the skin of one of the donors used in this study is in line with other studies. Berg et al. (13) described a large inter-individual variation in dimer-repair capacities among the volunteers used. Stimulation of DNA repair may be especially important in individuals that display little to no repair. Young et al. (14) observed hardly any removal of dimers in human skin. The relationship between DNA repair and skin cancer is evident from the rare genetic disease xeroderma pigmentosum in which defective DNA repair results in a 1000-fold increase in skin cancer suscepti- bility (15). The photoprotective role of tanning seems obvious when comparing the induction of erythema in fair-skinned individuals, who burn easily, with that in darker-skinned people, who are less susceptible to sunburn. More importantly, darker-skinned indi- viduals are less at risk compared to fair-skinned individuals to develop skin cancer (16). The induction of DNA damage is one of the initiating molecular events underlying UV-induced mutagenesis, immunosuppression, and skin cancer (17,18). Melanin was recently shown to form supranuclear caps over nuclei, absorbing incoming light, and thereby reducing UV-induced DNA photoproducts in human epidermis (19). The re- duction in the formation of DNA damage occurred in a melanin concentration- dependent manner. Besides this obvious inverse relationship between melanin and photoproduct induction, a possible link between melanin synthesis and induction and/or repair of DNA damage