The prevalence of antibiotics poses a serious challenge to biological nitrogen removal in wastewater. In this study, the effects of sulfamethoxazole and/or trimethoprim (15 mg/L∼30 mg/L) on treatment performance, nitrogen transformation and antibiotic resistance genes (ARGs) were investigated in aerobic activated sludge systems to elucidate the metabolic mechanism under high antibiotic stress. 15 mg/L single antibiotic stress improved total nitrogen removal performance due to the persistence of nitrifiers and enrichment of denitrifiers, with an optimum removal efficiency of 96.5 %. Up-regulation of all denitrifying genes, coupled with enhanced electron transfer of Complex II and III, contributed to the emergence of aerobic denitrification. The increased expression of antioxidant genes also alleviated intracellular pressure. Whereas combined antibiotic stress induced the significant down-regulation of denitrifying bacteria and genes (nirKS and nosZ), and suppressed the electron supply for denitrification by restraining genes related to Complex Ⅰ and energy supply by tricarboxylic acid cycle, driving the collapse of activated sludge system, with ammonia and total nitrogen removal efficiencies dropping to below 40 % and 20 %, respectively. The dominant genera in system changed from TM7a to Thiothrix and Sphaerotilus with increasing antibiotic concentration and type. Moreover, antibiotic stress promoted a slight enrichment of ARGs, especially those encoding efflux mechanisms. Cooperative relationships (> 93 %) dominated among ARGs, and Klebsiella was identified as the crucial host. ARGs regulating antibiotic efflux were more likely to be co-expressed with functional genes. These results may provide a theoretical basis for establishing promising strategies to mitigate antibiotic-caused process deterioration.

中文翻译：

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对磺胺甲噁唑和/或甲氧苄啶胁迫驱动的好氧活性污泥系统中氮转化、电子流和抗生素抗性基因的协同响应机制的分子生态学见解


抗生素的普遍存在对废水中的生物脱氮构成了严峻挑战。本研究研究了磺胺甲噁唑和/或甲氧苄啶 （15 mg/L∼30 mg/L） 对好氧活性污泥系统中处理性能、氮转化和抗生素耐药基因 （ARG） 的影响，以阐明高抗生素胁迫下的代谢机制。由于硝化剂的持久性和反硝化剂的富集，15 mg/L 单一抗生素胁迫提高了总氮去除性能，最佳去除效率为 96.5 %。所有反硝化基因的上调，加上复合物 II 和 III 的增强电子转移，促进了好氧反硝化的出现。抗氧化基因表达的增加也缓解了细胞内压力。而抗生素联合胁迫诱导了反硝化细菌和基因 （nirKS 和 nosZ） 的显著下调，并通过抑制与复合物 I. 相关的基因和三羧酸循环的能量供应来抑制反硝化的电子供应，导致活性污泥系统的崩溃，氨和总氮的去除效率下降到 40 % 和 20 % 以下， 分别。随着抗生素浓度和类型的增加，系统中的优势属从 TM7a 变为 Thiothrix 和 Sphaerotilus。此外，抗生素应激促进了 ARGs 的轻微富集，尤其是那些编码外排机制的 ARGs。合作关系 （> 93 %） 在 ARGs 中占主导地位，克雷伯菌被确定为关键宿主。调节抗生素外排的 ARGs 更可能与功能基因共表达。 这些结果可能为建立有前途的策略来减轻抗生素引起的过程恶化提供理论基础。