Among numerous engineered nanoparticles (NPs), CuNPs have been identified as a kind of high-risk inhibitor to anammox bacteria; however, the potential effects of salinity on the toxicity of CuNPs to anammox consortia remain unclear. Their short-term and long-term effects on anammox consortia were investigated by batch assays and continuously-fed bioreactors. The addition of 5.0–7.4 g L⁻¹ NaCl immediately shielded the acute inhibition of 2.0–4.6 mg L⁻¹ CuNPs on anammox activity. However, the coexistence of 5.0 g L⁻¹ NaCl significantly aggravated the inhibitory effect of 3.0 mg L⁻¹ CuNPs on anammox activity after exposure of about one month through reducing the content of extracellular polysaccharides. Even, the membrane permeability was significantly increased with the further increase of NaCl to 8.0 g L⁻¹. Although the relative abundance of anammox bacteria at the DNA level was relatively higher, most of the anammox cells may not be able to perform metabolic functions normally due to membrane damage. Thus, appropriate salinity would attenuate the adverse impacts caused by the short-term shock of CuNPs, while pre-treatment is required to avoid the synergistic stress of high CuNPs when treating high salt wastewater.

中文翻译：

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盐度通过调节细胞外聚合物物质和膜通透性来改变铜纳米颗粒对厌氧氨氧化物质的毒性


在众多工程纳米颗粒 （NPs） 中，CuNPs 已被确定为一种厌氧氨氧化菌的高危抑制剂;然而，盐度对 CuNPs 对厌氧氨氧化联盟的毒性的潜在影响仍不清楚。通过批量测定和连续进料生物反应器研究了它们对厌氧氨氧化联盟的短期和长期影响。添加 5.0-7.4 g ^L-1 NaCl 立即屏蔽了 2.0-4.6 mg ^L-1 CuNP 对厌氧氨氧化活性的急性抑制。然而，5.0 g ^L-1 NaCl 的共存通过降低细胞外多糖的含量，显着加剧了 3.0 mg ^L-1 CuNPs 在暴露约一个月后对厌氧氨氧化活性的抑制作用。甚至，随着 NaCl 的进一步增加至 8.0 g ^L-1，膜通透性显着增加。虽然厌氧氨氧化菌在 DNA 水平上的相对丰度相对较高，但由于膜损伤，大多数厌氧氨氧化细胞可能无法正常执行代谢功能。因此，适当的盐度可以减轻 CuNPs 短期冲击造成的不利影响，同时在处理高盐废水时需要进行预处理以避免高 CuNPs 的协同应力。