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自腐蚀微电解强化对向扩散生物膜系统中同步去除氨氮、磺胺甲恶唑和抗生素抗性基因。

Simultaneous removal of ammonia nitrogen, sulfamethoxazole, and antibiotic resistance genes in self-corrosion microelectrolysis-enhanced counter-diffusion biofilm system.

机构信息

State Key Laboratory of Urban Water Resource and Environment (SKLUWRE), Harbin Institute of Technology, 73 Huanghe Road, Nangang District, Harbin 150090, PR China.

State Key Laboratory of Urban Water Resource and Environment (SKLUWRE), Harbin Institute of Technology, 73 Huanghe Road, Nangang District, Harbin 150090, PR China.

出版信息

Bioresour Technol. 2024 Nov;412:131399. doi: 10.1016/j.biortech.2024.131399. Epub 2024 Aug 31.

DOI:10.1016/j.biortech.2024.131399
PMID:39218364
Abstract

A self-corrosion microelectrolysis (SME)-enhanced membrane-aerated biofilm reactor (eMABR) was developed for the removal of pollutants and reduction of antibiotic resistance genes (ARGs). Fe and Fe formed iron oxides on the biofilm, which enhanced the adsorption and redox process. SME can induce microorganisms to secrete more extracellular proteins and up-regulate the expression of ammonia monooxygenase (AMO) (0.92 log). AMO exposed extra binding sites (ASP-69) for antibiotics, weakening the competition between NH-N and sulfamethoxazole (SMX). The NH-N removal efficiency in the S-eMABR (adding SMX and IC) increased by 44.87 % compared to the S-MABR (adding SMX). SME increased the removal performance of SMX by approximately 1.45 times, down-regulated the expressions of sul1 (-1.69 log) and sul2 (-1.30 log) genes, and controlled their transfer within the genus. This study provides a novel strategy for synergistic reduction of antibiotics and ARGs, and elucidates the corresponding mechanism based on metatranscriptomic and molecular docking analyses.

摘要

一种自腐蚀微电解(SME)增强型膜曝气生物膜反应器(eMABR)被开发用于去除污染物和减少抗生素抗性基因(ARGs)。Fe 和 Fe 在生物膜上形成氧化铁,增强了吸附和氧化还原过程。SME 可以诱导微生物分泌更多的细胞外蛋白,并上调氨单加氧酶(AMO)的表达(0.92 log)。AMO 为抗生素暴露了更多的结合位点(ASP-69),削弱了 NH-N 和磺胺甲恶唑(SMX)之间的竞争。与 S-MABR(添加 SMX 和 IC)相比,S-eMABR(添加 SMX)中的 NH-N 去除效率提高了 44.87%。SME 将 SMX 的去除性能提高了约 1.45 倍,下调了 sul1(-1.69 log)和 sul2(-1.30 log)基因的表达,并控制了它们在属内的转移。本研究提供了一种协同减少抗生素和 ARGs 的新策略,并基于宏转录组学和分子对接分析阐明了相应的机制。

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