布洛芬对硫自性脱过程和微生物毒性反应机制的影响
Nengyao Xu1, Haibo Li2, Tingting Guo3
1School of Civil Engineering and Architecture, Taizhou University, Taizhou 318000, Zhejiang, China; School of Environmental and Municipal Engineering, Tianjin Key Laboratory of Aquatic Science and Technology, Tianjin Chengjian University, Tianjin 300384, China.
Bioresource technology
|June 5, 2023
概括
高度的布洛芬 (IBU) 通过破坏微生物细胞来抑制硫自脱 (SAD). 然而,低IBU度可以刺激微生物活动和电子转移,揭示了hormesis有毒反应机制.
科学领域:
- 环境微生物学 环境微生物学
- 生物技术是生物技术.
- 环境化学环境化学
背景情况:
- 硫自脱 (SAD) 对于废水处理中的酸盐去除至关重要.
- 了解像布洛芬 (IBU) 这样的药物对微生物过程的影响对于环境保护至关重要.
- 在SAD微生物群落上IBU的毒理机制需要进一步阐明.
研究的目的:
- 为了研究不同度的布洛芬对硫自脱 (SAD) 过程的影响.
- 为了阐明微生物有毒反应机制,在SAD期间暴露在伊布罗芬.
- 为了确定在布洛芬压力下,SAD过程中是否存在霍梅西斯效应.
主要方法:
- 硫自性脱 (SAD) 批量实验使用不同度 (1,10和50毫克/升) 的布洛芬 (IBU) 进行.
- 对酸盐去除效率进行了监测.
- 微生物氧化应激通过电化学表征和尼古丁胺氨基二核酸 (NADH) 和酸还原酶活性分析来评估.
主要成果:
- 高IBU度 (10和50 mg/L) 显著抑制了酸盐去除性能.
- 低IBU度 (1 mg/L) 显示对酸盐去除的影响微不足道,但诱导了微生物自我保护的基本氧化应激.
- 高IBU度诱导高强度氧化应激,损害微生物细胞膜,抑制电子转移,并降低代谢活性.
结论:
- 布洛芬在SAD过程中表现出度依赖的毒性作用.
- 低度的IBU可能会诱导一种hormesis效应,刺激微生物活动,而高度是有害的.
- 该研究提出了SAD过程中对ibuprofen暴露的hormesis毒性反应机制,强调了制药污染控制的重要性.
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