Abstract：
This review article is aimed at providing updated information on the contribution of immediate and delayed oxidative reactions to the photo-induced damage to cellular DNA/skin under exposure to UVB/UVA radiations and visible light. Low-intensity UVC and UVB radiations that operate predominantly through direct excitation of the nucleobases are very poor oxidizing agents giving rise to very low amounts of 8-oxo-7,8-dihydroguanine and DNA strand breaks with respect to the overwhelming bipyrimidine dimeric photoproducts. The importance of these two classes of oxidatively generated damage to DNA significantly increases together with a smaller contribution of oxidized pyrimidine bases upon UVA irradiation. This is rationalized in terms of sensitized photooxidation reactions predominantly mediated by singlet oxygen together with a small contribution of hydroxyl radical that appear to also be implicated in the photodynamic effects of the blue light component of visible light. Chemiexcitation-mediated formation of \"dark\" cyclobutane pyrimidine dimers in UVA-irradiated melanocytes is a recent major discovery that implicates in the initial stage, a delayed generation of reactive oxygen and nitrogen species giving rise to triplet excited carbonyl intermediate and possibly singlet oxygen. High-intensity UVC nanosecond laser radiation constitutes a suitable source of light to generate pyrimidine and purine radical cations in cellular DNA via efficient biphotonic ionization.
摘要：
本文旨在提供有关在暴露于UVB/UVA辐射和可见光下，立即和延迟的氧化反应对光诱导的细胞DNA/皮肤损伤的贡献的最新信息。主要通过直接激发核碱基起作用的低强度UVC和UVB辐射是非常差的氧化剂，相对于压倒性的联嘧啶二聚体光产物，会产生非常低量的8-氧代-7,8-二氢鸟嘌呤和DNA链断裂。在UVA照射下，这两类氧化产生的DNA损伤的重要性显着增加，而氧化嘧啶碱基的贡献较小。就主要由单线态氧介导的敏化光氧化反应以及羟基自由基的少量贡献而言，这是合理的，羟基自由基似乎也与可见光的蓝光成分的光动力效应有关。在UVA照射的黑素细胞中，化学激发介导的“暗”环丁烷嘧啶二聚体的形成是最近的一项重大发现，涉及初始阶段。活性氧和氮物质的延迟产生，产生三重态激发的羰基中间体和可能的单线态氧。高强度UVC纳秒激光辐射构成了合适的光源，可通过有效的双光子电离在细胞DNA中产生嘧啶和嘌呤自由基阳离子。
