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细菌产生的硫化氢驱动肠道微生物群落中的隐匿氧化还原化学。

Bacterial hydrogen sulfide drives cryptic redox chemistry in gut microbial communities.

机构信息

Department of Systems and Computational Biology, Albert Einstein College of Medicine, Bronx, NY, USA.

Departments of Medicine and Cell Biology, Albert Einstein College of Medicine, Bronx, NY, USA.

出版信息

Nat Metab. 2022 Oct;4(10):1260-1270. doi: 10.1038/s42255-022-00656-z. Epub 2022 Oct 20.

DOI:10.1038/s42255-022-00656-z
PMID:36266544
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11328334/
Abstract

Microbial biochemistry contributes to a dynamic environment in the gut. Yet, how bacterial metabolites such as hydrogen sulfide (HS) mechanistically alter the gut chemical landscape is poorly understood. Here we show that microbially generated HS drives the abiotic reduction of azo (R-N = N-R') xenobiotics, which are commonly found in Western food dyes and drugs. This nonenzymatic reduction of azo compounds is demonstrated in Escherichia coli cultures, in human faecal microbial communities and in vivo in male mice. Changing dietary levels of the HS xenobiotic redox partner Red 40 transiently decreases mouse faecal sulfide levels, demonstrating that a xenobiotic can attenuate sulfide concentration and alleviate HS accumulation in vivo. Cryptic HS redox chemistry thus can modulate sulfur homeostasis, alter the chemical landscape in the gut and contribute to azo food dye and drug metabolism. Interactions between chemicals derived from microbial communities may be a key feature shaping metabolism in the gut.

摘要

微生物生物化学有助于肠道形成动态环境。然而,细菌代谢物(如硫化氢(HS))如何在机制上改变肠道化学环境还知之甚少。在这里,我们表明微生物产生的 HS 驱动了偶氮(R-N ═ N-R')外源性物质的非酶还原,这些物质通常存在于西方食品染料和药物中。这种偶氮化合物的非酶还原在大肠杆菌培养物、人类粪便微生物群落以及雄性小鼠体内得到了证实。改变 HS 外源性氧化还原伴侣 Red 40 的饮食水平会短暂降低小鼠粪便中的硫化物水平,这表明外源性物质可以降低硫化物浓度并减轻体内 HS 的积累。因此,隐匿的 HS 氧化还原化学可以调节硫稳态,改变肠道内的化学环境,并有助于偶氮食品染料和药物的代谢。源自微生物群落的化学物质之间的相互作用可能是塑造肠道代谢的关键特征。

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本文引用的文献

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The Capacity to Produce Hydrogen Sulfide (HS) via Cysteine Degradation Is Ubiquitous in the Human Gut Microbiome.通过半胱氨酸降解产生硫化氢(HS)的能力在人类肠道微生物群中普遍存在。
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