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). Fe2+ and Fe3+ 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 log2). AMO exposed extra binding sites (ASP-69) for antibiotics, weakening the competition between NH4+-N and sulfamethoxazole (SMX). The NH4+-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 log2) and sul2 (−1.30 log2) 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.

中文翻译：

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自腐蚀微电解增强反扩散生物膜系统同时去除氨氮、磺胺甲恶唑和抗生素抗性基因


开发了一种自腐蚀微电解（SME）增强型膜曝气生物膜反应器（eMABR），用于去除污染物和减少抗生素抗性基因（ARG）。 Fe2+和Fe3+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胞外蛋白并上调氨单加氧酶（AMO）的表达（0.92 log2）。 AMO 暴露了额外的抗生素结合位点 (ASP-69)，削弱了 NH4+-N 和磺胺甲恶唑 (SMX) 之间的竞争。与S-MABR（添加SMX）相比，S-eMABR（添加SMX和IC）的NH4+-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 log2）和sul2（-1.30 log2）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ARG的新策略，并基于宏转录组和分子对接分析阐明了相应的机制。