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肠道中依赖硫化物和亚硝酸盐的一氧化氮生成。

Sulfide- and nitrite-dependent nitric oxide production in the intestinal tract.

机构信息

Laboratory of Microbial Ecology and Technology, Ghent University, Coupure Links 653, B-9000 Gent, Belgium.

出版信息

Microb Biotechnol. 2012 May;5(3):379-87. doi: 10.1111/j.1751-7915.2011.00320.x. Epub 2011 Nov 29.

DOI:10.1111/j.1751-7915.2011.00320.x
PMID:22129449
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3821680/
Abstract

In the gut ecosystem, nitric oxide (NO) has been described to have damaging effects on the energy metabolism of colonocytes. Described mechanisms of NO production are microbial reduction of nitrate via nitrite to NO and conversion of l-arginine by NO synthase. The aim of this study was to investigate whether dietary compounds can stimulate the production of NO by representative cultures of the human intestinal microbiota and whether this correlates to other processes in the intestinal tract. We have found that the addition of a reduced sulfur compound, i.e. cysteine, contributed to NO formation. This increase was ascribed to higher sulfide concentrations generated from cysteine that in turn promoted the chemical conversion of nitrite to NO. The NO release from nitrite was of the order of 4‰ at most. Overall, it was shown that two independent biological processes contribute to the chemical formation of NO in the intestinal tract: (i) the production of sulfide by fermentation of sulfur containing amino acids or reduction of sulfate by sulfate reducing bacteria, and (ii) the reduction of nitrate to nitrite. Our results indicate that dietary thiol compounds in combination with nitrate may contribute to colonocytes damaging processes by promoting NO formation.

摘要

在肠道生态系统中,一氧化氮(NO)被描述为对结肠细胞的能量代谢具有破坏性影响。描述的 NO 产生机制是微生物通过亚硝酸盐将硝酸盐还原为 NO,以及通过一氧化氮合酶将 l-精氨酸转化为 NO。本研究的目的是调查膳食化合物是否可以刺激人类肠道微生物群代表性培养物产生 NO,以及这是否与肠道内的其他过程相关。我们发现,添加还原硫化合物,即半胱氨酸,有助于形成 NO。这种增加归因于半胱氨酸产生的更高浓度的硫化物,硫化物反过来又促进了亚硝酸盐向 NO 的化学转化。亚硝酸盐释放的 NO 最多达到 4‰。总的来说,结果表明,两个独立的生物学过程有助于肠道中 NO 的化学形成:(i)含硫氨基酸发酵或硫酸盐还原菌还原硫酸盐产生的硫化物,以及(ii)硝酸盐还原为亚硝酸盐。我们的结果表明,饮食中的硫醇化合物与硝酸盐结合可能通过促进 NO 形成而导致结肠细胞损伤过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd6/3821680/903e82573495/mbt0005-0379-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd6/3821680/743ee03b3a59/mbt0005-0379-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd6/3821680/4a06a832d8fd/mbt0005-0379-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd6/3821680/34bfe59451cb/mbt0005-0379-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd6/3821680/d653e33d354c/mbt0005-0379-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd6/3821680/903e82573495/mbt0005-0379-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd6/3821680/743ee03b3a59/mbt0005-0379-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd6/3821680/4a06a832d8fd/mbt0005-0379-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd6/3821680/34bfe59451cb/mbt0005-0379-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd6/3821680/d653e33d354c/mbt0005-0379-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd6/3821680/903e82573495/mbt0005-0379-f5.jpg

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