Abstract

Photochemical reactions in cell DNA are induced in various organisms by solar UV radiation and may lead to a series of biological responses to DNA damage, including apoptosis, mutagenesis, and carcinogenesis. The chemical nature and the amount of DNA lesions depend on the wavelength of UV radiation. UV type B (UVB, 290–320 nm) causes two main lesions, cyclobutane pyrimidine dimers (CPDs) and, with a lower yield, pyrimidine (6-4) pyrimidone photoproducts (6-4PPs). Their formation is a result of direct UVB photon absorption by DNA bases. UV type A (UVA, 320–400 nm) induces only cyclobutane dimers, which most likely arise via triplet–triplet energy transfer (TTET) from cell chromophores to DNA thymine bases. UVA is much more effective than UVB in inducing sensitized oxidative DNA lesions, such as single-strand breaks and oxidized bases. Of the latter, 8-oxo-dihydroguanine (8-oxodG) is the most frequent, being produced in several oxidation processes. Many recent studies reported novel, more detailed information about the molecular mechanisms of the photochemical reactions that underlie the formation of various DNA lesions. The information is mostly summarized and analyzed in the review. Special attention is paid to the oxidation reactions that are initiated by reactive oxygen species (ROS) and radicals generated by potential endogenous photosensitizers, such as pterins, riboflavin, protoporphyrin IX, NADH, and melanin. The review discusses the role that specific DNA photoproducts play in genotoxic processes induced in living systems by UV radiation of various wavelengths, including human skin carcinogenesis.

中文翻译：

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不同波长紫外线辐射损伤细胞 DNA 的光化学过程：生物学后果

摘要

太阳紫外线辐射在多种生物体中诱导细胞DNA中的光化学反应，并可能导致一系列针对DNA损伤的生物反应，包括细胞凋亡、诱变和癌变。DNA 损伤的化学性质和数量取决于紫外线辐射的波长。B 型 UV（UVB，290–320 nm）会引起两种主要损伤：环丁烷嘧啶二聚体 (CPD) 和产量较低的嘧啶 (6-4) 嘧啶酮光产物 (6-4PP)。它们的形成是 DNA 碱基直接吸收 UVB 光子的结果。A 型紫外线（UVA，320–400 nm）仅诱导环丁烷二聚体，这种二聚体很可能是通过从细胞发色团到 DNA 胸腺嘧啶碱基的三重态-三重态能量转移 (TTET) 产生的。UVA 在诱导敏感氧化 DNA 损伤（例如单链断裂和氧化碱基）方面比 UVB 更有效。其中，8-氧代-二氢鸟嘌呤 (8-oxodG) 是最常见的，在多种氧化过程中产生。最近的许多研究报告了关于光化学反应分子机制的新颖、更详细的信息，这些光化学反应是各种 DNA 损伤形成的基础。综述中主要对信息进行总结和分析。特别关注由活性氧 (ROS) 和潜在内源性光敏剂（如蝶呤、核黄素、原卟啉 IX、NADH 和黑色素）产生的自由基引发的氧化反应。该综述讨论了特定 DNA 光产物在生命系统中由各种波长的紫外线辐射诱导的基因毒性过程中所发挥的作用，包括人类皮肤癌的发生。