Wang S Q, Setlow R, Berwick M, Polsky D, Marghoob A A, Kopf A W, Bart R S
Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York, NY 10016, USA.
J Am Acad Dermatol. 2001 May;44(5):837-46. doi: 10.1067/mjd.2001.114594.
The incidence and mortality rates of melanoma have risen for many decades in the United States. Increased exposure to ultraviolet (UV) radiation is generally considered to be responsible. Sunburns, a measure of excess sun exposure, have been identified as a risk factor for the development of melanoma. Because sunburns are primarily due to UVB (280-320 nm) radiation, UVB has been implicated as a potential contributing factor to the pathogenesis of melanoma. The adverse role of UVA (320-400 nm) in this regard is less well studied, and currently there is a great deal of controversy regarding the relationship between UVA exposure and the development of melanoma. This article reviews evidence in the English-language literature that surrounds the controversy concerning a possible role for UVA in the origin of melanoma. Our search found that UVA causes DNA damage via photosensitized reactions that result in the production of oxygen radical species. UVA can induce mutations in various cultured cell lines. Furthermore, in two animal models, the hybrid Xiphophorus fish and the opossum (Mondelphis domestica), melanomas and melanoma precursors can be induced with UVA. UVA radiation has been reported to produce immunosuppression in laboratory animals and in humans. Some epidemiologic studies have reported an increase in melanomas in users of sunbeds and sunscreens and in patients exposed to psoralen and UVA (PUVA) therapy. There is basic scientific evidence of the harmful effects of UVA on DNA, cells and animals. Collectively, these data suggest a potential role for UVA in the pathogenesis of melanoma. To date evidence from epidemiologic studies and clinical observations are inconclusive but seem to be consistent with this hypothesis. Additional research on the possible role of UVA in the pathogenesis of melanoma is required.
在美国,黑色素瘤的发病率和死亡率几十年来一直在上升。紫外线(UV)辐射暴露增加通常被认为是罪魁祸首。晒伤是过度日晒的一种衡量指标,已被确定为黑色素瘤发生的一个危险因素。由于晒伤主要是由UVB(280 - 320纳米)辐射引起的,UVB被认为是黑色素瘤发病机制的一个潜在促成因素。UVA(320 - 400纳米)在这方面的不利作用研究较少,目前关于UVA暴露与黑色素瘤发生之间的关系存在大量争议。本文综述了英文文献中围绕UVA在黑色素瘤起源中可能作用的争议的证据。我们的研究发现,UVA通过光敏反应导致DNA损伤,从而产生氧自由基。UVA可在各种培养细胞系中诱导突变。此外,在两种动物模型,即杂交剑尾鱼和负鼠(短尾负鼠)中,UVA可诱发黑色素瘤和黑色素瘤前体。据报道,UVA辐射会在实验动物和人类中产生免疫抑制。一些流行病学研究报告称,使用日光浴床和防晒霜的人群以及接受补骨脂素和UVA(PUVA)治疗的患者中黑色素瘤有所增加。有基础科学证据表明UVA对DNA、细胞和动物具有有害影响。总体而言,这些数据表明UVA在黑色素瘤发病机制中可能发挥作用。迄今为止,流行病学研究和临床观察的证据尚无定论,但似乎与这一假设一致。需要对UVA在黑色素瘤发病机制中的可能作用进行更多研究。