Elucidating microbial iron corrosion mechanisms with a hydrogenase-deficient strain of Desulfovibrio vulgaris.

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
{"title":"Elucidating microbial iron corrosion mechanisms with a hydrogenase-deficient strain of <i>Desulfovibrio vulgaris</i>.","authors":"Di Wang, Toshiyuki Ueki, Peiyu Ma, Dake Xu, Derek R Lovley","doi":"10.1002/mlf2.12133","DOIUrl":null,"url":null,"abstract":"<p><p>Sulfate-reducing microorganisms extensively contribute to the corrosion of ferrous metal infrastructure. There is substantial debate over their corrosion mechanisms. We investigated Fe<sup>0</sup> corrosion with <i>Desulfovibrio vulgaris</i>, the sulfate reducer most often employed in corrosion studies. Cultures were grown with both lactate and Fe<sup>0</sup> as potential electron donors to replicate the common environmental condition in which organic substrates help fuel the growth of corrosive microbes. Fe<sup>0</sup> was corroded in cultures of a <i>D. vulgaris</i> hydrogenase-deficient mutant with the 1:1 correspondence between Fe<sup>0</sup> loss and H<sub>2</sub> accumulation expected for Fe<sup>0</sup> oxidation coupled to H<sup>+</sup> reduction to H<sub>2</sub>. This result and the extent of sulfate reduction indicated that <i>D. vulgaris</i> was not capable of direct Fe<sup>0</sup>-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 H<sub>2</sub> removal was not necessary for the enhanced corrosion observed in the presence of microbes. The parental H<sub>2</sub>-consuming strain corroded more Fe<sup>0</sup> than the mutant strain, which could be attributed to H<sub>2</sub> oxidation coupled to sulfate reduction, producing sulfide that further stimulated Fe<sup>0</sup> oxidation. The results suggest that H<sub>2</sub> consumption is not necessary for microbially enhanced corrosion, but H<sub>2</sub> oxidation can indirectly promote corrosion by increasing sulfide generation from sulfate reduction. The finding that <i>D. vulgaris</i> was incapable of direct electron uptake from Fe<sup>0</sup> reaffirms that direct metal-to-microbe electron transfer has yet to be rigorously described in sulfate-reducing microbes.</p>","PeriodicalId":94145,"journal":{"name":"mLife","volume":"3 2","pages":"269-276"},"PeriodicalIF":4.5000,"publicationDate":"2024-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11211667/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"mLife","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1002/mlf2.12133","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/6/1 0:00:00","PubModel":"eCollection","JCR":"Q1","JCRName":"MICROBIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

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.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
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。
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。
求助全文
约1分钟内获得全文 去求助
来源期刊
CiteScore
2.30
自引率
0.00%
发文量
0
期刊最新文献
Staphylococcus aureus SOS response: Activation, impact, and drug targets. EmbB and EmbC regulate the sensitivity of Mycobacterium abscessus to echinomycin. Metabolic activities of marine ammonia-oxidizing archaea orchestrated by quorum sensing. Zinc finger 4 negatively controls the transcriptional activator Fzf1 in Saccharomyces cerevisiae. Efficient, compact, and versatile: Type I-F2 CRISPR-Cas system.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1