γ-射线和辐射诱导的串联 DNA 病变的突变和修复

DNA Pub Date : 2024-05-06 DOI:10.3390/dna4020009
A. Basu, Laureen C. Colis, J. H. T. Bacurio
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引用次数: 0

摘要

电离辐射会诱发多种不同类型的 DNA 损伤。但其特点之一是产生复杂的 DNA 损伤,其中串联 DNA 损伤因其独特的生物特性而备受关注。组织炎症引起的氧化应激以及产生自由基的金属催化反应也会形成这些 DNA 损伤。在本小视图中,我们总结了串联病变的形成以及在特定位点合成后对其进行的复制和修复研究。其中许多病变对传统的碱基切除修复具有抗性,因此只能通过核苷酸切除修复途径进行修复。它们还会阻碍 DNA 复制,当发生病变旁路时,可能会出现严重的错误。其中一些串联 DNA 病变可能会导致衰老、神经系统疾病和癌症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mutagenesis and Repair of γ-Radiation- and Radical-Induced Tandem DNA Lesions
Ionizing radiation induces many different types of DNA lesions. But one of its characteristics is to produce complex DNA damage, of which tandem DNA damage has received much attention, owing to its promise of distinctive biological properties. Oxidative stresses in response to inflammation in tissues and metal-catalyzed reactions that result in generation of radicals also form these DNA lesions. In this minireview, we have summarized the formation of the tandem lesions as well as the replication and repair studies carried out on them after site-specific synthesis. Many of these lesions are resistant to the traditional base excision repair, so that they can only be repaired by the nucleotide excision repair pathway. They also block DNA replication and, when lesion bypass occurs, it may be significantly error-prone. Some of these tandem DNA lesions may contribute to ageing, neurological diseases, and cancer.
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DNA
DNA
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