首页> 外文OA文献 >The Thiol:Disulfide Oxidoreductase DsbB Mediates the Oxidizing Effects of the Toxic Metalloid Tellurite (TeO32−) on the Plasma Membrane Redox System of the Facultative Phototroph Rhodobacter capsulatus▿
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The Thiol:Disulfide Oxidoreductase DsbB Mediates the Oxidizing Effects of the Toxic Metalloid Tellurite (TeO32−) on the Plasma Membrane Redox System of the Facultative Phototroph Rhodobacter capsulatus▿

机译:硫醇:二硫键氧化还原酶DsbB介导有毒准金属碲酸盐(TeO32-)对兼性光养性荚膜红细菌的质膜氧化还原系统的氧化作用

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摘要

The highly toxic oxyanion tellurite (TeO32−) is a well known pro-oxidant in mammalian and bacterial cells. This work examines the effects of tellurite on the redox state of the electron transport chain of the facultative phototroph Rhodobacter capsulatus, in relation to the role of the thiol:disulfide oxidoreductase DsbB. Under steady-state respiration, the addition of tellurite (2.5 mM) to membrane fragments generated an extrareduction of the cytochrome pool (c- and b-type hemes); further, in plasma membranes exposed to tellurite (0.25 to 2.5 mM) and subjected to a series of flashes of light, the rate of the QH2:cytochrome c (Cyt c) oxidoreductase activity was enhanced. The effect of tellurite was blocked by the antibiotics antimycin A and/or myxothiazol, specific inhibitors of the QH2:Cyt c oxidoreductase, and, most interestingly, the membrane-associated thiol:disulfide oxidoreductase DsbB was required to mediate the redox unbalance produced by the oxyanion. Indeed, this phenomenon was absent from R. capsulatus MD22, a DsbB-deficient mutant, whereas the tellurite effect was present in membranes from MD22/pDsbBWT, in which the mutant gene was complemented to regain the wild-type DsbB phenotype. These findings were taken as evidence that the membrane-bound thiol:disulfide oxidoreductase DsbB acts as an “electron conduit” between the hydrophilic metalloid and the lipid-embedded Q pool, so that in habitats contaminated with subinhibitory amounts of TeIV, the metalloid is likely to function as a disposal for the excess reducing power at the Q-pool level of facultative phototrophic bacteria.
机译:高毒性的氧阴离子亚碲酸盐(TeO32-)是哺乳动物和细菌细胞中众所周知的促氧化剂。这项工作检查了硫柳石对荚膜红养细菌荚膜红细菌的电子传输链的氧化还原状态的影响,与硫醇:二硫化物氧化还原酶DsbB的作用有关。在稳态呼吸下,向膜碎片中添加亚碲酸盐(2.5 mM)会导致细胞色素库(c型和b型血红素)的减少。此外,在暴露于亚碲酸盐(0.25至2.5 mM)并经受一系列闪光的质膜中,QH2:细胞色素c(Cyt c)氧化还原酶活性的速率得到提高。碲化物的作用被抗生素抗霉素A和/或甲噻唑,QH2:Cyt c氧化还原酶的特定抑制剂所阻断,最有趣的是,膜相关的硫醇:二硫键氧化还原酶DsbB可以介导由氧化膜产生的氧化还原不平衡。氧阴离子。实际上,DsbB缺陷型突变体荚膜梭菌MD22中不存在这种现象,而MD22 / pDsbBWT的膜中存在亚碲酸盐效应,其中突变基因被补充以恢复野生型DsbB表型。这些发现被证明是膜结合的巯基:二硫键氧化还原酶DsbB充当亲水性类金属与脂质包埋的Q库之间的“电子导管”,因此在被亚抑制量的TeIV污染的栖息地中,类金属很可能作为兼性光养细菌在Q池水平上过量还原能力的处置。

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