Berking C
Klinik und Poliklinik für Dermatologie und Allergologie der Ludwig-Maximilians-Universität München.
Hautarzt. 2005 Jul;56(7):687-96; quiz 697. doi: 10.1007/s00105-005-0984-8.
The incidence of melanoma has been rising during the past 40 years and may be the result of lifestyle changes that have led to an increased sun exposure in fair-skinned people. Ultraviolet radiation (UVR) is believed to be the main causative factor in melanoma development with an acute intermittent exposure being more relevant than a chronic cumulative one. While UVB (280-320 nm) can directly cause DNA damage (UVB fingerprint mutations) in the cells of the epidermis, UVA (320-400 nm) induces damage indirectly by the formation of reactive oxygen species. Since UV-associated mutations are rare in melanoma, it is speculated that UVR supports melanoma development by indirect effects, e.g. immunosuppression or stimulation of growth factors in the skin. Taken together, animal models and epidemiological data suggest a UVA-associated pathogenesis of melanoma that puts into question the effectiveness of sunscreens in melanoma prevention.
在过去40年中，黑色素瘤的发病率一直在上升，这可能是生活方式改变导致皮肤白皙的人日晒增加的结果。紫外线辐射（UVR）被认为是黑色素瘤发生的主要致病因素，急性间歇性暴露比慢性累积暴露更具相关性。虽然UVB（280-320纳米）可直接导致表皮细胞中的DNA损伤（UVB指纹突变），但UVA（320-400纳米）通过活性氧的形成间接诱导损伤。由于紫外线相关突变在黑色素瘤中很少见，推测UVR通过间接作用支持黑色素瘤的发展，例如免疫抑制或刺激皮肤中的生长因子。综合来看，动物模型和流行病学数据表明黑色素瘤与UVA相关的发病机制，这对防晒霜在预防黑色素瘤方面的有效性提出了质疑。
