Suppr超能文献

同步短程硝化-厌氧氨氧化-反硝化(SNAD)系统对 Zn(II)暴露的新认识:聚焦于影响群体感应对外界电子传递和微生物代谢的调控。

New insights of simultaneous partial nitritation, anammox and denitrification (SNAD) system to Zn(II) exposure: Focus on affecting the regulation of quorum sensing on extracellular electron transfer and microbial metabolism.

机构信息

School of Environmental and Municipal Engineering, Tianjin Key Laboratory of Aquatic Science and Technology, Tianjin Chengjian University, Tianjin 300384, China.

School of Environmental and Municipal Engineering, Tianjin Key Laboratory of Aquatic Science and Technology, Tianjin Chengjian University, Tianjin 300384, China.

出版信息

Bioresour Technol. 2022 Feb;346:126602. doi: 10.1016/j.biortech.2021.126602. Epub 2021 Dec 23.

Abstract

Here, the toxicity responses mechanism of the simultaneous partial nitritation, anammox and denitrification (SNAD) system to Zn(II) exposure were explored with emphasis on the repressed quorum sensing (QS) regulation on extracellular electron transfer and microbial metabolism. Results showed that Zn(II) accumulated in cells and induced oxidative stress, which led to microbial structure destruction. The increased electron transfer impedance and reduced redox substances (flavin/Cytochrome c) implied that Zn(II) affected electron transfer. The decreased ATP level, dehydrogenase and nitrogen related enzymatic activities showed Zn(II) affected organic matter and nitrogen metabolism. Furthermore, combined with Pearson network analysis, Zn(II) exposure disturbed the QS to decrease Acyl Homoserine Lactones (AHLs) secretion responsible for regulating extracellular electron transfer and microbial metabolism, thereby disturbing the performance of the SNAD system. This study provided new insights into the toxicity responses mechanism of the SNAD system to HM exposure.

摘要

本文重点研究了同时亚硝化-厌氧氨氧化-反硝化(SNAD)系统对 Zn(II)暴露的毒性响应机制,强调了群体感应(QS)对胞外电子传递和微生物代谢的抑制调节作用。结果表明,Zn(II)在细胞内积累并诱导氧化应激,导致微生物结构破坏。电子传递阻抗的增加和氧化还原物质(黄素/Cytochrome c)的减少表明 Zn(II)影响了电子传递。ATP 水平、脱氢酶和氮相关酶活性的降低表明 Zn(II)影响了有机物和氮代谢。此外,结合 Pearson 网络分析,Zn(II)暴露干扰了 QS,减少了负责调节胞外电子传递和微生物代谢的酰基高丝氨酸内酯(AHLs)的分泌,从而干扰了 SNAD 系统的性能。本研究为 SNAD 系统对重金属暴露的毒性响应机制提供了新的见解。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验