The manganese and iron superoxide dismutases protect Escherichia coli from heavy metal toxicity
The manganese and iron superoxide dismutases protect Escherichia coli from heavy metal toxicity
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DOI：
10.1016/s0923-2508(01)01273-6
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发表时间：
2001-12-01
影响因子：
2.6
通讯作者：
Jeanthon, C
中科院分区：
文献类型：
--
作者：
Geslin, C;Llanos, J;Jeanthon, C
超氧化物歧化酶（SOD）是通过分解超氧自由基来抵抗氧化应激的重要组成部分。大肠杆菌含有两种高度同源的SOD，一种含锰酶和一种含铁酶（分别为Mn-SOD和Fe-SOD）。相比之下，枯草芽孢杆菌中存在单一的Mn-SOD。在大肠在大肠杆菌中，SOD的缺失与对镉、镍和钴离子的敏感性增加有关。缺乏sodA或sodB的突变体表现出与野生型菌株相当的金属抗性水平。虽然sod缺陷的突变体细胞更耐锌比他们的野生型对应，没有观察到在铜的存在下菌株之间的差异。在B。sodA突变对镉和铜抗性没有影响。这些结果表明，镉、镍和钴在大肠杆菌细胞内产生的超氧阴离子是有毒的。杆菌他们支持sod基因参与其对金属胁迫的保护。(C)2001年，Elsevier SAS科学与医学版。
Superoxide dismutases (SODs) are vital components that defend against oxidative stress through decomposition of superoxide radical. Escherichia coli contains two highly homologous SODs, a manganese- and an iron-containing enzyme (Mn-SOD and Fe-SOD, respectively). In contrast, a single Mn-SOD is present in Bacillus subtilis. In E. coli, the absence of SODs was found to be associated with an increased sensitivity to cadmium, nickel and cobalt ions. Mutants lacking either sodA or sodB exhibited metal resistance to levels comparable to that of the wild-type strain. Although sod-deficient mutant cells were more resistant to zinc than their wild-type counterpart, no differences between the strains were observed in the presence of copper. In B. subtilis, the sodA mutation had no effect on cadmium and copper resistance. These results suggest that intracellular generation of superoxide by cadmium, nickel and cobalt is toxic in E. coli. They support the participation of sod genes in its protection against metal stress. (C) 2001 Editions scientifiques et medicales Elsevier SAS.