Wassberg Cecilia, Bäckvall Helena, Diffey Brian, Pontén Fredrik, Berne Berit
Department of Medical Sciences/Dermatology and Venereology, University Hospital, Uppsala, Sweden.
Acta Derm Venereol. 2003;83(4):254-61. doi: 10.1080/00015550310016481.
The p53 protein plays a key role in protecting cells from acquiring manifest mutations by inducing cell cycle arrest or apoptosis. The mechanisms for differences in epidermal responses to ultraviolet irradiation are unclear, although they have been shown to be related to both genetic events and environmental factors. In this study, we compared epidermal ultraviolet responses in chronically sun-exposed and non-sun-exposed skin using immunohistochemistry with antibodies recognizing thymine dimers and p53 protein. Six healthy volunteers were subjected to both artificial ultraviolet irradiation and natural sunlight, with and without photoprotection. A smaller number of thymine dimer-positive keratinocytes were detected 24 h after ultraviolet exposure in chronically sun-exposed skin compared to non-sun-exposed skin. Further, the p53 response was more variable in chronically sun-exposed skin. A significant correlation between total ultraviolet dose and number of p53-immunoreactive keratinocytes was found after natural sun exposure. Our findings suggest that repair of DNA damage is more efficient in chronically sun-exposed skin than in non-sun-exposed skin.
p53蛋白在通过诱导细胞周期停滞或凋亡来保护细胞避免发生明显突变方面发挥着关键作用。尽管已表明表皮对紫外线照射的反应差异机制与遗传事件和环境因素均有关，但目前尚不清楚。在本研究中，我们使用识别胸腺嘧啶二聚体和p53蛋白的抗体进行免疫组织化学，比较了长期暴露于阳光下和未暴露于阳光下的皮肤的表皮紫外线反应。六名健康志愿者接受了人工紫外线照射和自然阳光照射，有或没有光保护措施。与未暴露于阳光下的皮肤相比，长期暴露于阳光下的皮肤在紫外线照射24小时后检测到的胸腺嘧啶二聚体阳性角质形成细胞数量较少。此外，长期暴露于阳光下的皮肤中p53反应的变异性更大。自然阳光照射后，总紫外线剂量与p53免疫反应性角质形成细胞数量之间存在显著相关性。我们的研究结果表明，长期暴露于阳光下的皮肤中DNA损伤的修复比未暴露于阳光下的皮肤更有效。
