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活性氧和脂质过氧化产物所导致的DNA损伤的加合物形成、诱变作用及核苷酸切除修复

Adduct formation, mutagenesis and nucleotide excision repair of DNA damage produced by reactive oxygen species and lipid peroxidation product.

作者信息

Møller P, Wallin H

机构信息

National Institute of Occupational Health, Lerso Parkallé 105, DK-2100 Copenhagen O, Denmark.

出版信息

Mutat Res. 1998 Jun;410(3):271-90. doi: 10.1016/s1383-5742(97)00041-0.

Abstract

Reactive oxygen species are formed constantly in living organisms, as products of the normal metabolism, or as a result of many different environmental influences. Here we review the knowledge of formation of DNA damage, the mutations caused by reactive oxygen species and the role of the excision repair processes, that protect the organism from oxidative DNA damage. In particular, we have focused on recent studies that demonstrate the important role of nucleotide excision repair. We propose two major roles of nucleotide excision repair as 1) a backup when base excision repair of small oxidative lesions becomes saturated, and as 2) a primary repair pathway for DNA damage produced by lipid peroxidation products.

摘要

活性氧作为正常新陈代谢的产物或多种不同环境影响的结果,在生物体内不断形成。在此,我们综述了有关DNA损伤的形成、活性氧引起的突变以及切除修复过程的作用的知识,这些切除修复过程可保护生物体免受氧化性DNA损伤。特别是,我们重点关注了近期那些证明核苷酸切除修复重要作用的研究。我们提出核苷酸切除修复的两个主要作用为:1)当小的氧化性损伤的碱基切除修复饱和时作为一种备用机制;2)作为脂质过氧化产物产生的DNA损伤的主要修复途径。

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