A hydrogen-oxidizing bacterium Ideonella sp. TH17 was investigated for ammonium removal from wastewater. Possible pathways and mechanisms of nitrogen assimilation under the stress of two typical quinolone antibiotics and their mixture were studied by molecular biological approaches. The results showed that the capability of ammonium assimilation by TH17 was stimulated at lower concentration (5 μg/L), but inhibited at elevated concentration of quinolone antibiotics. The inhibitory effect of mixed antibiotics was weaker than that of individual antibiotics at higher concentration. Under stress of 5 μg/L quinolone antibiotics, the expression of ammonium assimilation genes was up-regulated, and activities of functional and antioxidant enzymes were enhanced. Meanwhile, the expression of antibiotic resistance gene was up-regulated, which increased the tolerance of TH17 to quinolone antibiotics. Further, amino acid, purine and biotin metabolisms were up-regulated significantly to provide energy, substrates, and coenzymes for enhanced nitrogen metabolism of TH17. Therefore, the influencing pathways and mechanisms of low-concentration quinolone antibiotics on nitrogen removal by TH17 were revealed by gene, enzyme and metabolite molecules, which could guide the development and application of novel processes for biological nitrogen removal from wastewater.

针对一株氢氧化细菌Ideonella sp. TH17进行污水生物脱氨氮研究, 并应用分子生物学技术解析两种典型喹诺酮类抗生素及其混合物对TH17氨同化的影响途径和机理。结果表明, 低浓度(5 μg/L)喹诺酮类抗生素对TH17脱氮性能具有促进作用, 浓度升高则出现抑制作用, 混合抗生素削弱了高浓度抗生素对TH17脱氮性能的抑制作用。在5 μg/L喹诺酮类抗生素胁迫下, TH17氨同化基因表达上调, 氨同化酶和抗氧化系统酶活性提升。同时, TH17抗性基因表达上调, 增加了细胞的抗生素耐受性。进一步地, TH17胞内氨基酸、嘌呤和生物素代谢等通路显著上调, 为氮代谢提供能量、底物和辅酶, 最终提升了氨同化性能。研究结果从基因、酶和代谢物分子水平上揭示了低浓度喹诺酮类抗生素对TH17脱氮性能的影响途径与机理, 可为污水生物脱氮新技术的开发和应用提供理论支撑。