Berbis P
Clinique Dermatologique, Hôtel-Dieu, Marseille.
Rev Fr Gynecol Obstet. 1991 Jun;86(6):448-50.
A variety of clinical, topographical, histological, epidemiological and geographical arguments attribute to the effects of solar radiation and to ultraviolet rays (UV) in particular, a decisive role in the processes of cutaneous carcinogenesis. This carcinogenicity is part of a series of chronic changes affecting the integument which constitute heliodermatitis or photosenescence. The effects of UV are cumulative. DNA is the main target of UV rays. Man possesses several DNA repair systems. The hereditary malfunction of part of these systems result in xeroderma pigmentosum, which constitutes a pathological model of photocarcinogenesis. Intrinsic skin ageing (non-photodependent) appears to promote this process of photocarcinogenicity by several mechanisms: summation of DNA changes, progressive deterioration of repair systems, dermal-epidermal atrophy, melanocytic changes, immuno-surveillance deficit.
多种临床、局部解剖学、组织学、流行病学及地理学证据表明,太阳辐射尤其是紫外线(UV)在皮肤癌发生过程中起决定性作用。这种致癌性是影响皮肤的一系列慢性变化的一部分,这些变化构成了日光性皮炎或光老化。紫外线的影响具有累积性。DNA是紫外线的主要靶点。人类拥有多种DNA修复系统。这些系统部分的遗传性故障会导致色素性干皮病,这构成了光致癌作用的病理模型。皮肤内在老化(非光依赖性)似乎通过多种机制促进这种光致癌过程:DNA变化的累加、修复系统的逐渐退化、真皮-表皮萎缩、黑素细胞变化、免疫监视缺陷。