Solar ultraviolet radiation (UVR) induces DNA damage in human epidermis especially the cyclobutane pyrimidine dimer (CPD) that may lead to skin cancer, the incidence of which is much lower in black compared with white skin. It is assumed that melanin inhibits skin cancer by preventing CPD formation, but we lack quantitative data.
We compared CPD in black and white skins after acute erythemally equivalent exposures of solar simulated radiation (SSR). CPD were assessed in three zones: basal, mid and upper epidermis [1]. A quantitative analysis showed a strong relationship between CPD and melanin concentration. The high concentration of melanin in the basal layer offered a CPD protection factor of 59 compared with 5 in the upper epidermis with the least melanin. Importantly, the basal layer is the region that contains keratinocyte stem cells and melanocytes. The level of CPD protection by melanin in the basal layer is comparable to differences in skin cancer incidence in black and white skins and provides indirect evidence that melanin reduces skin cancer incidence by inhibiting CPD.
SSR can also induce “dark” CPD which are formed after the end of exposure [2]. There is evidence that melanin carbonyls act as sensitisers for “dark” CPD formation [3]. White skin showed a similar “dark” CPD distribution in the three epidermal zones described above. In contrast in black skin there was a high prevalence of “dark” CPD in the upper epidermis, some in the mid epidermis but none in the basal layer. This suggests that melanin may sensitise or inhibit “dark” CPD depending on its concentration.