利用氢化酶缺陷的普通脱硫弧菌菌株阐明微生物的铁腐蚀机制。

IF 4.5 Q1 MICROBIOLOGY
mLife Pub Date : 2024-06-28 eCollection Date: 2024-06-01 DOI:10.1002/mlf2.12133
Di Wang, Toshiyuki Ueki, Peiyu Ma, Dake Xu, Derek R Lovley
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引用次数: 0

摘要

硫酸盐还原微生物广泛造成黑色金属基础设施的腐蚀。关于它们的腐蚀机制还存在大量争议。我们研究了硫酸盐还原菌(Desulfovibrio vulgaris)对 Fe0 的腐蚀,它是腐蚀研究中最常用的硫酸盐还原菌。培养物以乳酸盐和 Fe0 作为潜在的电子供体,以复制有机底物有助于腐蚀性微生物生长的常见环境条件。在一种 D. vulgaris 氢酶缺陷突变体的培养物中,Fe0 被腐蚀,Fe0 氧化与 H+ 还原成 H2 的过程中,Fe0 损失与 H2 积累的比例为 1:1。这一结果和硫酸盐还原的程度表明,即使在大量硫化亚铁存在的情况下为 D. vulgaris 提供了补充能源,它也无法实现 Fe0 到微生物的直接电子传递。氢化酶缺乏的突变体培养物的腐蚀程度高于无菌对照组,这表明在有微生物存在的情况下,H2的去除并不是增强腐蚀的必要条件。亲本消耗 H2 的菌株比突变菌株腐蚀更多的 Fe0,这可能是由于 H2 氧化与硫酸盐还原耦合,产生了进一步刺激 Fe0 氧化的硫化物。结果表明,微生物增强腐蚀并不需要消耗 H2,但 H2 氧化可通过增加硫酸盐还原产生的硫化物来间接促进腐蚀。发现 D. vulgaris 无法直接从 Fe0 吸收电子再次证明,在硫酸盐还原微生物中,金属与微生物之间的直接电子传递尚未得到严格描述。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Elucidating microbial iron corrosion mechanisms with a hydrogenase-deficient strain of Desulfovibrio vulgaris.

Sulfate-reducing microorganisms extensively contribute to the corrosion of ferrous metal infrastructure. There is substantial debate over their corrosion mechanisms. We investigated Fe0 corrosion with Desulfovibrio vulgaris, the sulfate reducer most often employed in corrosion studies. Cultures were grown with both lactate and Fe0 as potential electron donors to replicate the common environmental condition in which organic substrates help fuel the growth of corrosive microbes. Fe0 was corroded in cultures of a D. vulgaris hydrogenase-deficient mutant with the 1:1 correspondence between Fe0 loss and H2 accumulation expected for Fe0 oxidation coupled to H+ reduction to H2. This result and the extent of sulfate reduction indicated that D. vulgaris was not capable of direct Fe0-to-microbe electron transfer even though it was provided with a supplementary energy source in the presence of abundant ferrous sulfide. Corrosion in the hydrogenase-deficient mutant cultures was greater than in sterile controls, demonstrating that H2 removal was not necessary for the enhanced corrosion observed in the presence of microbes. The parental H2-consuming strain corroded more Fe0 than the mutant strain, which could be attributed to H2 oxidation coupled to sulfate reduction, producing sulfide that further stimulated Fe0 oxidation. The results suggest that H2 consumption is not necessary for microbially enhanced corrosion, but H2 oxidation can indirectly promote corrosion by increasing sulfide generation from sulfate reduction. The finding that D. vulgaris was incapable of direct electron uptake from Fe0 reaffirms that direct metal-to-microbe electron transfer has yet to be rigorously described in sulfate-reducing microbes.

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