{"title":"Photochemical Processes of Cell DNA Damage by UV Radiation of Various Wavelengths: Biological Consequences","authors":"G. Ya. Fraikin, N. S. Belenikina, A. B. Rubin","doi":"10.1134/s0026893324010047","DOIUrl":null,"url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>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.</p>","PeriodicalId":18734,"journal":{"name":"Molecular Biology","volume":null,"pages":null},"PeriodicalIF":1.5000,"publicationDate":"2024-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular Biology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1134/s0026893324010047","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
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.
摘要太阳紫外线辐射在各种生物体内诱导细胞 DNA 发生光化学反应，并可能导致一系列 DNA 损伤生物反应，包括细胞凋亡、诱变和致癌。DNA 损伤的化学性质和数量取决于紫外线辐射的波长。B 型紫外线（UVB，290-320 纳米）主要导致两种病变，即环丁烷嘧啶二聚体（CPDs）和产量较低的嘧啶（6-4）嘧啶酮光致产物（6-4PPs）。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 纳米）只能诱导环丁烷二聚体，这种二聚体很可能是通过细胞发色团与 DNA 胸腺嘧啶碱基之间的三重-三重能量转移（TTET）产生的。在诱导敏化氧化 DNA 病变（如单链断裂和氧化碱基）方面，UVA 比 UVB 更有效。在后者中，8-氧代二氢鸟嘌呤（8-oxodG）是最常见的，它是在几个氧化过程中产生的。最近的许多研究报告了有关光化学反应分子机制的新颖、更详细的信息，这些信息是各种 DNA 病变形成的基础。本综述主要对这些信息进行了总结和分析。其中特别关注了由活性氧（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。这篇综述讨论了特定 DNA 光致产物在各种波长的紫外线辐射诱导生物系统（包括人类皮肤致癌）的基因毒性过程中发挥的作用。
期刊介绍：
Molecular Biology is an international peer reviewed journal that covers a wide scope of problems in molecular, cell and computational biology including genomics, proteomics, bioinformatics, molecular virology and immunology, molecular development biology, molecular evolution and related areals. Molecular Biology publishes reviews, experimental and theoretical works. Every year, the journal publishes special issues devoted to most rapidly developing branches of physical-chemical biology and to the most outstanding scientists.
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