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皮肤由表皮和真皮组成,表皮的干细胞称为基底细胞,它有活跃的分裂和分化能力,形成表皮的各个层面,构成了皮肤的新陈代谢。许多发色团[能够吸收紫外线辐射(ultraviolet radiation,UVR)并产生有害活性氧的化学物质]存在于皮肤中。DNA吸收户外紫外线(ultraviolet radiation B,UVB)光,引起相邻嘧啶碱基之间的变化,这些受损的DNA分子可以刺激引起皮肤炎症反应的修复机制。皮肤内的其他发色团吸收来自紫外光的光子并产生单线态氧,单线态氧是一种具有高度活性的氧类物质,反过来可以产生活性氧(reactive oxygen species,ROS),并组合起来攻击细胞组分,如细胞膜、细胞蛋白、脂质、核和线粒体DNA。辐射作用时,组织内产生大量的ROS自由基,会损伤蛋白质、脂质和核酸等生物大分子,引发一系列的炎症反应,抑制基底细胞的分裂分化,导致基底细胞及新生血管的丧失,从而产生皮肤损伤[1]。太阳辐射是指到达地球表面的连续的电磁辐射,包括部分紫外线和可见光。其中紫外线波长为200~400 nm,可见光波长为400~ 800 nm,紫外线又可分为短波紫外线(UVC,200~ 290 nm)、中波紫外线(UVB,290~320 nm)和长波紫外线(UVA,320~ 400 nm)。其中UVC对生命细胞的杀伤能力最强,但一般均被地面大气层中的氧及臭氧所吸收,因此,到达地面的紫外线主要是UVA和UVB,所以UVA和UVB是导致皮肤损伤的主要作用光谱。在3种不同波长的紫外线中,UVA导致细胞自由基生成、脂质过氧化的能力最强,可影响真皮组织中的胶原及弹力纤维,导致皮肤光老化;UVA的穿透力强,它对DNA损伤没有直接的影响,但它会间接地产生ROS,从而导致DNA氧化性损伤而致单链及双链的断裂。对于暴露于UVA辐射下并存在有光产物和DNA损伤的会继发引起光敏反应。UVB主要引起表皮层及真皮浅层的病变,UVR的能量通常被细胞中的蛋白质和DNA所吸收并引起多种DNA损伤,UVB由于本身的波长多被表皮的角质形成细胞所吸收而引起DNA损伤,从而产生日晒红斑、免疫抑制及皮肤癌。可见光可促进表皮皮肤替代物中ROS及炎症因子如IL-1α、IL-6、IL-8、粒细胞-巨噬细胞集落刺激因子(granulocyte-Macrophage colony-stimulating factor,GM-CSF)的产生,增加金属基质蛋白酶的表达,但不能促进肿瘤坏死因子α的释放。此外,可见光可激活表皮生长因子受体-细胞外调节蛋白激酶(epidermal growth factor receptor-extracellular regulated protein kinases,EGFR-ERK)信号调节通路。太阳辐射造成的皮肤损伤是皮肤癌的主要风险因素。太阳辐射导致的皮肤癌的发病率在肤色白皙的人群中较高,特别是在欧洲人群中更为显著,这与皮肤对阳光敏感性的基因有关。晒黑反应主要由黑色素的色素沉着决定,旨在保护皮肤免受DNA损伤。在这篇综述中,我们主要关注紫外线等光源对皮肤损伤、黑素瘤和皮肤癌的影响,还讨论了与其相关的基因位点及局部策略的临床新应用。
太阳辐射对皮肤损伤及其损伤机制的研究进展
Research Progress on Mechanism of skin damage and injury induced by solar radiation
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摘要: 近年来,皮肤癌特别是鳞状细胞癌的发生率明显上升,并呈年轻化趋势,据报道,90%的皮肤癌与紫外线辐射损伤有关。太阳光谱中的紫外线,特别是户外紫外线(290~320 nm)和长波黑斑效应紫外线(320~400 nm)刺激皮肤后,表皮黑素细胞通过合成黑素,转移至邻近的角质形成细胞,对皮肤起光保护作用。皮肤受到过量紫外线刺激后会出现一系列损伤反应,包括晒黑及炎症反应、细胞DNA损伤、光致癌作用等。近年来,研究发现可见光(400~700 nm)和臭氧同样可造成皮肤损伤。而环境暴露造成的皮肤损伤主要是由活性氧的产生引起对蛋白质、脂质和核酸等细胞组分的氧化损伤,进而引起皮肤内部复杂的一系列反应。这些受损的皮肤细胞引发炎症反应,导致皮肤出现最终损伤。因此,进一步掌握光致皮肤损伤的机制及正确的辐射防护措施,对相关疾病的治疗及预防有着重要的临床指导意义。笔者对太阳光包括紫外线、可见光和臭氧对皮肤损伤的影响以及太阳辐射对皮肤晒黑的基因位点的研究进行了总结描述,旨在探究预防和治疗太阳辐射引起皮肤损伤的新途径。Abstract: In recent years, the incidence of skin cancer, especially squamous cell carcinoma, has increased significantly. About 90% of skin cancers are associated with ultraviolet radiation damage. Upon exposure of the skin to ultraviolet rays, especially UVB (290–320 nm) and UVA (320–400 nm), epidermal melanocytes migrate to adjacent keratinocytes by synthesizing melanin, thus providing light protection for the skin. A series of damage reactions, including tanning and inflammation, cell DNA damage, and photocarcinogenesis, occurred after the skin was stimulated by excessive ultraviolet radiation. Recent studies have found that visible light (400–700 nm) and ozone can also cause skin damage. The skin damage caused by environmental exposure is mainly attributed to the production of reactive oxygen species, which cause oxidative damage to protein, lipid, and nucleic acid, followed by a series of complex reactions within the skin. Damaged skin cells cause inflammatory reactions, resulting in ultimate damage to the skin. Therefore, understanding the mechanism of photoinduced skin damage and developing correct radiation protection measures are important for the treatment and prevention of related diseases. This review summarizes the effects of sunlight, including ultraviolet, visible, and ozone on skin damage, as well as the research on gene loci of suntan caused by sunlight, to explore new ways to prevent and treat skin damage caused by solar radiation.
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Key words:
- Solar radiation /
- Skin damage /
- Gene loci /
- Antioxidation
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