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紫外线B(UVB)和紫外线A(UVA)辐射对细胞DNA产生的氧化损伤。

Oxidatively generated damage to cellular DNA by UVB and UVA radiation.

作者信息

Cadet Jean, Douki Thierry, Ravanat Jean-Luc

机构信息

University Grenoble Alpes, INAC, Grenoble, France; CEA, INAC, Grenoble, France; Département de Médecine Nucléaire et Radiobiologie, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, Sherbrooke, QC, Canada.

出版信息

Photochem Photobiol. 2015 Jan-Feb;91(1):140-55. doi: 10.1111/php.12368. Epub 2014 Nov 27.

DOI:10.1111/php.12368
PMID:25327445
Abstract

This review article focuses on a critical survey of the main available information on the UVB and UVA oxidative reactions to cellular DNA as the result of direct interactions of UV photons, photosensitized pathways and biochemical responses including inflammation and bystander effects. UVA radiation appears to be much more efficient than UVB in inducing oxidatively generated damage to the bases and 2-deoxyribose moieties of DNA in isolated cells and skin. The UVA-induced generation of 8-oxo-7,8-dihydroguanine is mostly rationalized in terms of selective guanine oxidation by singlet oxygen generated through type II photosensitization mechanism. In addition, hydroxyl radical whose formation may be accounted for by metal-catalyzed Haber-Weiss reactions subsequent to the initial generation of superoxide anion radical contributes in a minor way to the DNA degradation. This leads to the formation of both oxidized purine and pyrimidine bases together with DNA single-strand breaks at the exclusion, however, of direct double-strand breaks. No evidence has been provided so far for the implication of delayed oxidative degradation pathways of cellular DNA. In that respect putative characteristic UVA-induced DNA damage could include single and more complex lesions arising from one-electron oxidation of the guanine base together with aldehyde adducts to amino-substituted nucleobases.

摘要

这篇综述文章重点批判性地审视了关于紫外线B(UVB)和紫外线A(UVA)与细胞DNA发生氧化反应的主要现有信息,这些反应是紫外线光子直接相互作用、光敏化途径以及包括炎症和旁观者效应在内的生化反应的结果。在分离的细胞和皮肤中,UVA辐射在诱导对DNA碱基和2-脱氧核糖部分的氧化损伤方面似乎比UVB更有效。UVA诱导产生8-氧代-7,8-二氢鸟嘌呤主要归因于通过II型光敏化机制产生的单线态氧对鸟嘌呤的选择性氧化。此外,超氧阴离子自由基最初生成后,金属催化的哈伯-维伊斯反应可能导致羟基自由基的形成,它对DNA降解的贡献较小。这导致氧化嘌呤和嘧啶碱基的形成以及DNA单链断裂,但不包括直接的双链断裂。到目前为止,尚未有证据表明细胞DNA存在延迟氧化降解途径。在这方面,推测的UVA诱导的DNA损伤可能包括鸟嘌呤碱基单电子氧化产生的单一和更复杂的损伤以及氨基取代核碱基的醛加合物。

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