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肠道细菌产生的硫化氢可能会引发帕金森病。

Hydrogen Sulfide Produced by Gut Bacteria May Induce Parkinson's Disease.

机构信息

Institute of Clinical Medicine, University of Eastern Finland (UEF), 70211 Kuopio, Finland.

出版信息

Cells. 2022 Mar 12;11(6):978. doi: 10.3390/cells11060978.

Abstract

Several bacterial species can generate hydrogen sulfide (HS). Study evidence favors the view that the microbiome of the colon harbors increased amounts of HS producing bacteria in Parkinson's disease. Additionally, HS can easily penetrate cell membranes and enter the cell interior. In the cells, excessive amounts of HS can potentially release cytochrome c protein from the mitochondria, increase the iron content of the cytosolic iron pool, and increase the amount of reactive oxygen species. These events can lead to the formation of alpha-synuclein oligomers and fibrils in cells containing the alpha-synuclein protein. In addition, bacterially produced HS can interfere with the body urate metabolism and affect the blood erythrocytes and lymphocytes. Gut bacteria responsible for increased HS production, especially the mucus-associated species of the bacterial genera belonging to the Desulfovibrionaceae and Enterobacteriaceae families, are likely play a role in the pathogenesis of Parkinson's disease. Special attention should be devoted to changes not only in the colonic but also in the duodenal microbiome composition with regard to the pathogenesis of Parkinson's disease. Influenza infections may increase the risk of Parkinson's disease by causing the overgrowth of HS-producing bacteria both in the colon and duodenum.

摘要

一些细菌物种可以产生硫化氢 (HS)。研究证据表明,帕金森病患者的结肠微生物群中产生 HS 的细菌数量增加。此外,HS 可以轻易穿透细胞膜并进入细胞内部。在细胞内,过量的 HS 可能会从线粒体中释放细胞色素 c 蛋白,增加细胞质铁池的铁含量,并增加活性氧物质的数量。这些事件可能导致含有α-突触核蛋白的细胞中α-突触核蛋白寡聚物和纤维的形成。此外,细菌产生的 HS 可以干扰体内尿酸代谢,并影响血液红细胞和淋巴细胞。导致 HS 产生增加的肠道细菌,特别是属于脱硫弧菌科和肠杆菌科的细菌属的黏液相关物种,可能在帕金森病的发病机制中发挥作用。应特别注意不仅在结肠而且在十二指肠微生物组组成方面发生的变化,以了解帕金森病的发病机制。流感感染可能会通过在结肠和十二指肠中过度生长产生 HS 的细菌来增加患帕金森病的风险。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e666/8946538/98cc35c8dcb5/cells-11-00978-g001.jpg

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