论文标题：The Terminal Oxidase Cytochrome bd Promotes Sulfide-resistant Bacterial Respiration and Growth

期刊：Scientific Reports

作者：Elena Forte, Vitaliy B. Borisov, Micol Falabella, Henrique G. Colaço, Mariana Tinajero-Trejo, Robert K. Poole, João B. Vicente, Paolo Sarti & Alessandro Giuffrè

发表时间： 2016/03/31

数字识别码：10.1038/srep23788

原文链接：https://www.nature.com/articles/srep23788?utm_source=Other_website&utm_medium=Website_links&utm_content=RenLi-Nature-Scientific_Reports-Microbiology-China&utm_campaign=SCIREP_USG_rlp8212_Cytochrome_sciencenet_article_June_4th

《科学报告》发表的一项研究The Terminal Oxidase Cytochrome bd Promotes Sulfide-resistant Bacterial Respiration and Growth表明，细胞色素bd氧化酶对于耐硫细菌的有氧呼吸与增殖具有重要作用。

硫化氢(H2S)通过抑制血红素-铜离子型细胞色素c氧化酶的活性进而抑制线粒体呼吸。但是，包括大肠杆菌在内的许多原核生物却会在人类肠道中产生H2S，并长期生活于高浓度的H2S环境中。意大利国家研究会的Alessandro Giuffrè及其同事根据这一现象，试验了细菌能否在硫化物环境中保持有氧呼吸。

大肠杆菌的呼吸链末端具有3种氧化酶，血红素-铜离子型bo3氧化酶（对氰化物敏感）与2种细胞色素bd氧化酶（对氰化物不敏感）。作者针对这3种酶分别做了研究，他们发现3种氧化酶对硫化物的耐受程度差异明显，bo3氧化酶对硫化物的半抑制浓度只有1.1±0.1 μM，而2种细胞色素bd氧化酶的半抑制浓度则达到了58 μM。

在硫化物环境中，只保留了bo3氧化酶的大肠杆菌突变株的有氧呼吸与增殖都受到了强烈抑制。而只保留了细胞色素bd氧化酶的2种突变株，则能够耐受高达至200 μM浓度的硫化物环境。相应的，在有利于细胞色素bd氧化酶表达的环境中，野生型大肠杆菌也表现出了对硫化物的抗性。

细胞色素bd氧化酶促进了大肠杆菌（可能还包括其他细菌）在硫化物环境中的有氧呼吸与增殖。使得大肠杆菌获得了对硫化物的抗性，其对于人类肠道菌群环境及其病理变化的影响值得进一步研究。

摘要：Hydrogen sulfide (H2S) impairs mitochondrial respiration by potently inhibiting the heme-copper cytochrome c oxidase. Since many prokaryotes, including Escherichia (E.) coli, generate H2S and encounter high H2S levels particularly in the human gut, herein we tested whether bacteria can sustain sulfide-resistant O2-dependent respiration. E. coli has three respiratory oxidases, the cyanide-sensitive heme-copper bo3 enzyme and two bd oxidases much less sensitive to cyanide. Working on the isolated enzymes, we found that, whereas the bo3 oxidase is inhibited by sulfide with half-maximal inhibitory concentration IC50 = 1.1 ± 0.1 μM, under identical experimental conditions both bd oxidases are insensitive to sulfide up to 58 μM. In E. coli respiratory mutants, both O2-consumption and aerobic growth proved to be severely impaired by sulfide when respiration was sustained by the bo3 oxidase alone, but unaffected by ≤200 μM sulfide when either bd enzyme acted as the only terminal oxidase. Accordingly, wild-type E. coli showed sulfide-insensitive respiration and growth under conditions favouring the expression of bd oxidases. In all tested conditions, cyanide mimicked the functional effect of sulfide on bacterial respiration. We conclude that bd oxidases promote sulfide-resistant O2-consumption and growth in E. coli and possibly other bacteria. The impact of this discovery is discussed.

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