de Gruijl F R
Department of Dermatology, University Medical Centre Utrecht, The Netherlands.
Eur J Cancer. 1999 Dec;35(14):2003-9. doi: 10.1016/s0959-8049(99)00283-x.
Ultraviolet (UV) radiation in sunlight is the most prominent and ubiquitous physical carcinogen in our natural environment. It is highly genotoxic but does not penetrate the body any deeper than the skin. Like all organisms regularly exposed to sunlight, the human skin is extremely well adapted to continuous UV stress. Well-pigmented skin is clearly better protected than white Caucasian skin. The sun-seeking habits of white Caucasians in developed countries are likely to have contributed strongly to the increase in skin cancer observed over the last century. Skin cancer is by far the most common type of cancer in the U.S.A. and Australia, which appears to be the result of an 'unnatural displacement' of people with sun-sensitive skin to sub-tropical regions. Although campaigns have been successful in informing people about the risks of sun exposure, general attitudes and behaviour do not yet appear to have changed to the extent that trends in skin cancer morbidity and the corresponding burden on public healthcare will be reversed. The relationship between skin cancer and regular sun exposure was suspected by physicians in the late 19th century, and subsequently substantiated in animal experiments in the early part of the 20th century. UV radiation was found to be highly genotoxic, and DNA repair proved to be crucial in fending off detrimental effects such as mutagenesis and cell death. In fact, around 1940 it was shown that the wavelength dependence of mutagenicity paralleled the UV absorption by DNA. In the 1970s research on UV carcinogenesis received a new impetus from the arising concern about a possible future depletion of the stratospheric ozone layer: the resulting increases in ambient UV loads were expected to raise skin cancer incidences. Epidemiological studies in the last decades of the 20th century have greatly refined our knowledge on the aetiology of skin cancers. Analyses of gene mutations in skin carcinomas have identified UV radiation as the cause. The relationship between the most fatal skin cancer, i.e. malignant melanoma and solar UV exposure is, however, still unclear and needs to be clarified to optimise preventive measures and minimise mortality from skin cancers.
阳光中的紫外线(UV)辐射是我们自然环境中最显著且普遍存在的物理致癌物。它具有高度的基因毒性,但不会穿透身体超过皮肤深度。与所有经常暴露在阳光下的生物一样,人类皮肤对持续的紫外线压力具有极强的适应性。色素沉着良好的皮肤显然比白种人的皮肤受到更好的保护。发达国家白种人热衷于晒太阳的习惯很可能在很大程度上导致了上个世纪皮肤癌发病率的上升。在美国和澳大利亚,皮肤癌是迄今为止最常见的癌症类型,这似乎是对阳光敏感皮肤人群“非自然迁移”到亚热带地区的结果。尽管相关宣传活动成功地让人们了解了阳光照射的风险,但总体态度和行为似乎尚未改变到足以扭转皮肤癌发病率趋势以及相应公共医疗负担的程度。19世纪末,医生们就怀疑皮肤癌与经常晒太阳之间的关系,随后在20世纪初的动物实验中得到了证实。紫外线辐射被发现具有高度的基因毒性,而DNA修复在抵御诸如诱变和细胞死亡等有害影响方面被证明至关重要。事实上,大约在1940年,人们发现诱变性的波长依赖性与DNA的紫外线吸收情况平行。20世纪70年代,由于人们开始担心平流层臭氧层未来可能出现的损耗,紫外线致癌研究获得了新的推动力:预计由此导致的环境紫外线负荷增加会提高皮肤癌发病率。20世纪最后几十年的流行病学研究极大地丰富了我们对皮肤癌病因的认识。对皮肤癌基因突变的分析已确定紫外线辐射是病因所在。然而,最致命的皮肤癌,即恶性黑色素瘤与太阳紫外线照射之间的关系仍不明确,需要进一步阐明,以优化预防措施并降低皮肤癌死亡率。