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发光杆菌铜锌超氧化物歧化酶(SODs)与人AP内切核酸酶在DNA修复及氧化应激下SOD缺陷型大肠杆菌中的协同作用。

Collaborative effects of Photobacterium CuZn superoxide dismutase (SODs) and human AP endonuclease in DNA repair and SOD-deficient Escherichia coli under oxidative stress.

作者信息

Kim Young Gon

机构信息

Biological Sciences, College of Natural Sciences, Chosun University, 375 Seosukdong Dongku, 501-759, Kwangju, South Korea.

出版信息

Free Radic Biol Med. 2004 Jan 15;36(2):173-9. doi: 10.1016/j.freeradbiomed.2003.10.004.

Abstract

The defenses against free radical damage include specialized repair enzymes that correct oxidative damage in DNA and detoxification systems such as superoxide dismutases (SODs). These defenses may be coordinated genetically as global responses. We hypothesized that the expression of SOD and DNA repair genes would inhibit DNA damage under oxidative stress. Therefore, protection of Escherichia coli mutants deficient in SOD and DNA repair genes (sod-, xth-, and nfo-) was demonstrated by transforming the mutant strain with a plasmid pYK9 that encoded Photobacterium leiognathi CuZnSOD and human AP endonuclease. The results show that survival rates were increased in sod+ xth- nfo+ cells compared with sod- xth- ape-, sod- xth- ape-, and sod+ xth- ape- cells under oxidative stress generated with 0.1 mM paraquat or 3 mM H2O2. The data suggest that, at the least, SOD and DNA repair enzymes may collaborate on protection and repair of damaged DNA. Additionally, both enzymes are required for protection against free radicals.

摘要

针对自由基损伤的防御机制包括专门用于修复DNA氧化损伤的修复酶以及诸如超氧化物歧化酶(SOD)等解毒系统。这些防御机制可能作为整体反应在基因层面上进行协调。我们推测,SOD和DNA修复基因的表达会在氧化应激下抑制DNA损伤。因此,通过用编码发光杆菌属CuZnSOD和人AP核酸内切酶的质粒pYK9转化突变菌株,证明了对缺乏SOD和DNA修复基因(sod-、xth-和nfo-)的大肠杆菌突变体具有保护作用。结果表明,在0.1 mM百草枯或3 mM过氧化氢产生的氧化应激下,与sod- xth- ape-、sod- xth- ape-和sod+ xth- ape-细胞相比,sod+ xth- nfo+细胞的存活率有所提高。数据表明,至少SOD和DNA修复酶可能协同作用以保护和修复受损DNA。此外,这两种酶都是抵御自由基所必需的。

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