Ichihashi M, Ueda M, Budiyanto A, Bito T, Oka M, Fukunaga M, Tsuru K, Horikawa T
Division of Dermatology, Graduate School of Medicine, Translational Medicine, School of Medicine, Kobe University, Kobe, Japan.
Toxicology. 2003 Jul 15;189(1-2):21-39. doi: 10.1016/s0300-483x(03)00150-1.
Solar radiation induces acute and chronic reactions in human and animal skin. Chronic repeated exposures are the primary cause of benign and malignant skin tumors, including malignant melanoma. Among types of solar radiation, ultraviolet B (290-320 nm) radiation is highly mutagenic and carcinogenic in animal experiments compared to ultraviolet A (320-400 nm) radiation. Epidemiological studies suggest that solar UV radiation is responsible for skin tumor development via gene mutations and immunosuppression, and possibly for photoaging. In this review, recent understanding of DNA damage caused by direct UV radiation and by indirect stress via reactive oxygen species (ROS) and DNA repair mechanisms, particularly nucleotide excision repair of human cells, are discussed. In addition, mutations induced by solar UV radiation in p53, ras and patched genes of non-melanoma skin cancer cells, and the role of ROS as both a promoter in UV-carcinogenesis and an inducer of UV-apoptosis, are described based primarily on the findings reported during the last decade. Furthermore, the effect of UV on immunological reaction in the skin is discussed. Finally, possible prevention of UV-induced skin cancer by feeding or topical use of antioxidants, such as polyphenols, vitamin C, and vitamin E, is discussed.
太阳辐射可在人类和动物皮肤中引发急性和慢性反应。长期反复暴露是良性和恶性皮肤肿瘤（包括恶性黑色素瘤）的主要成因。在各类太阳辐射中，与紫外线A（320 - 400纳米）辐射相比，紫外线B（290 - 320纳米）辐射在动物实验中具有高度致突变性和致癌性。流行病学研究表明，太阳紫外线辐射通过基因突变和免疫抑制导致皮肤肿瘤的发生，还可能导致光老化。在本综述中，我们将讨论对直接紫外线辐射以及通过活性氧（ROS）产生的间接应激所造成的DNA损伤，以及DNA修复机制，特别是人类细胞的核苷酸切除修复的最新认识。此外，主要基于过去十年间所报告的研究结果，描述了太阳紫外线辐射在非黑色素瘤皮肤癌细胞的p53、ras和patched基因中诱发的突变，以及ROS作为紫外线致癌作用的促进剂和紫外线诱导凋亡的诱导剂的作用。此外，还讨论了紫外线对皮肤免疫反应的影响。最后，探讨了通过摄入或局部使用抗氧化剂（如多酚、维生素C和维生素E）来预防紫外线诱导的皮肤癌的可能性。
