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厌氧氨氧化菌群落对高浓度铁酸亚铁纳米粒子的抑制响应及潜在的恢复机制。

Response of anammox consortia to inhibition from high ferroferric oxide nanoparticles concentration and potential recovery mechanism.

机构信息

National Engineering Laboratory for Advanced Municipal Wastewater Treatment and Reuse Technology, Key Laboratory of Beijing for Water Quality Science and Water Environment Recovery Engineering, Beijing 100124, China.

National Engineering Laboratory for Advanced Municipal Wastewater Treatment and Reuse Technology, Key Laboratory of Beijing for Water Quality Science and Water Environment Recovery Engineering, Beijing 100124, China.

出版信息

Bioresour Technol. 2024 Jun;402:130808. doi: 10.1016/j.biortech.2024.130808. Epub 2024 May 7.

DOI:10.1016/j.biortech.2024.130808
PMID:38723724
Abstract

The substantial discharge of ferroferric oxide nanoparticles (FeO NPs) into sewage threatens the survival of functional microorganisms in wastewater treatment. This study elucidated responses of anaerobic ammonium oxidation (anammox) consortia to inhibition from high FeO NPs concentration and recovery mechanisms. The nitrogen removal efficiency decreased by 20.3 % and recovered after 55 days under 1000 mg/L FeO NPs concentration. Toxicity was attributed to reactive oxygen species (ROS) production. The excessive ROS damaged membrane integrity, nitrogen metabolism, and DNA synthesis, resulting in the inhibition of anammox bacteria activity. However, recovery mechanisms of anammox consortia activity were activated in response to 1000 mg/L FeO NPs. The increase of heme oxygenase-1, thioredoxin, and nicotinamide adenine dinucleotide-quinone oxidoreductase genes alleviated oxidative stress. Furthermore, the activation of metabolic processes associated with membrane and DNA repair promoted recovery of anammox bacteria activity. This study provided new insights into NPs contamination and control strategies during anammox process.

摘要

大量的四氧化三铁纳米颗粒(FeO NPs)排入污水会威胁到污水处理中功能微生物的生存。本研究阐明了厌氧氨氧化(anammox)菌受高浓度 FeO NPs 抑制的反应和恢复机制。在 1000mg/L FeO NPs 浓度下,氮去除效率下降了 20.3%,55 天后恢复。毒性归因于活性氧(ROS)的产生。过量的 ROS 破坏了细胞膜的完整性、氮代谢和 DNA 合成,从而抑制了 anammox 菌的活性。然而,anammox 菌活性的恢复机制在 1000mg/L FeO NPs 下被激活。血红素加氧酶-1、硫氧还蛋白和烟酰胺腺嘌呤二核苷酸醌氧化还原酶基因的增加缓解了氧化应激。此外,与膜和 DNA 修复相关的代谢过程的激活促进了 anammox 菌活性的恢复。本研究为 anammox 过程中纳米颗粒污染和控制策略提供了新的见解。

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