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JMP134通过过硫化物双加氧酶氧化和硫化氢释放减轻硫烷脱氢酶缺失后的硫烷硫毒性。

JMP134 Alleviates Sulfane Sulfur Toxicity after the Loss of Sulfane Dehydrogenase through Oxidation by Persulfide Dioxygenase and Hydrogen Sulfide Release.

作者信息

Xin Yufeng, Wang Yaxin, Zhang Honglin, Wu Yu, Xia Yongzhen, Li Huanjie, Qu Xiaohua

机构信息

College of Life Sciences, Qufu Normal University, Qufu 273165, China.

State Key Laboratory of Microbial Technology, Shandong University, Qingdao 266237, China.

出版信息

Metabolites. 2023 Feb 2;13(2):218. doi: 10.3390/metabo13020218.

Abstract

An incomplete Sox system lacking sulfane dehydrogenase SoxCD may produce and accumulate sulfane sulfur when oxidizing thiosulfate. However, how bacteria alleviate the pressure of sulfane sulfur accumulation remains largely unclear. In this study, we focused on the bacterium JMP134, which contains a complete Sox system. When soxCD was deleted, this bacterium temporarily produced sulfane sulfur when oxidizing thiosulfate. Persulfide dioxygenase (PDO) in concert with glutathione oxidizes sulfane sulfur to sulfite. Sulfite can spontaneously react with extra persulfide glutathione (GSSH) to produce thiosulfate, which can feed into the incomplete Sox system again and be oxidized to sulfate. Furthermore, the deletion strain lacking PDO and SoxCD produced volatile HS gas when oxidizing thiosulfate. By comparing the oxidized glutathione (GSSG) between the wild-type and deletion strains, we speculated that HS is generated during the interaction between sulfane sulfur and the glutathione/oxidized glutathione (GSH/GSSG) redox couple, which may reduce the oxidative stress caused by the accumulation of sulfane sulfur in bacteria. Thus, PDO and HS release play a critical role in alleviating sulfane sulfur toxicity after the loss of soxCD in JMP134.

摘要

缺乏硫烷脱氢酶SoxCD的不完整Sox系统在氧化硫代硫酸盐时可能产生并积累硫烷硫。然而,细菌如何缓解硫烷硫积累的压力在很大程度上仍不清楚。在本研究中,我们聚焦于含有完整Sox系统的细菌JMP134。当soxCD被缺失后,该细菌在氧化硫代硫酸盐时会暂时产生硫烷硫。过硫化物双加氧酶(PDO)与谷胱甘肽协同作用将硫烷硫氧化为亚硫酸盐。亚硫酸盐可与额外的过硫化谷胱甘肽(GSSH)自发反应生成硫代硫酸盐,后者可再次进入不完整的Sox系统并被氧化为硫酸盐。此外,缺失PDO和SoxCD的缺失菌株在氧化硫代硫酸盐时会产生挥发性HS气体。通过比较野生型和缺失菌株之间的氧化型谷胱甘肽(GSSG),我们推测HS是在硫烷硫与谷胱甘肽/氧化型谷胱甘肽(GSH/GSSG)氧化还原对相互作用过程中产生的,这可能减轻细菌中硫烷硫积累引起的氧化应激。因此,PDO和HS释放对缓解JMP134中soxCD缺失后硫烷硫的毒性起着关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f9e/9959259/3ae1ef8bf0e6/metabolites-13-00218-g001.jpg

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