Wang Xiaohong, Kang Longfei, Li Tianjian, Wang Shanshan, Ma Haibo, Tian Yajun, Sun Jianqiang, Li Jun
College of Environment, Zhejiang University of Technology, Hangzhou 310014, China.
College of Environmental Science and Engineering, Zhejiang University of Water Resources and Electric Power, Hangzhou 310018, China.
Environ Sci Technol. 2025 Aug 5;59(30):15931-15943. doi: 10.1021/acs.est.5c01739. Epub 2025 Jul 24.
The redox dynamics of estuarine sediments critically influence the environmental fate of antibiotics, yet the mechanistic pathways under oxygen-fluctuating conditions have been insufficiently elucidated. This study elucidates the dual-function role of pyrite in mediating the oxidative and reductive degradation of three model antibiotics (sulfamethoxazole, SMX; norfloxacin, NOR; and chlortetracycline, CTC) under aerobic and anaerobic conditions. Systematic batch experiments coupled with reactive oxygen species analysis reveal a dual-function mechanism for pyrite involving oxidative degradation via OH under aerobic conditions and reductive transformation under anaerobic conditions. Notably, sulfur species in pyrite serve as key electron donors, driving the defluorination and dechlorination reactions of NOR and CTC in the absence of molecular oxygen. X-ray absorption fine structure along with density functional theory simulations further demonstrate an S-Fe-antibiotic electron transfer pathway, wherein sulfide donates electrons via Fe(II) coordination sites. Field validation using natural estuary sediments corroborates the laboratory findings, highlighting the substantial contribution of pyrite-mediated reductive pathways to antibiotic attenuation. These findings advance the mechanistic insight into pyrite-driven redox processes in estuarine environments and underscore the overlooked role of sulfur species in mediating nonradical antibiotic degradation, with implications for natural attenuation and remediation strategies in sulfur-rich coastal systems.
河口沉积物的氧化还原动力学严重影响抗生素的环境归宿，然而在氧气波动条件下的作用机制尚未得到充分阐明。本研究阐明了黄铁矿在有氧和厌氧条件下介导三种模型抗生素（磺胺甲恶唑，SMX；诺氟沙星，NOR；和金霉素，CTC）氧化和还原降解中的双重作用。系统的批次实验结合活性氧分析揭示了黄铁矿的双重作用机制，包括在有氧条件下通过OH进行氧化降解以及在厌氧条件下进行还原转化。值得注意的是，黄铁矿中的硫物种作为关键电子供体，在没有分子氧的情况下驱动NOR和CTC的脱氟和脱氯反应。X射线吸收精细结构以及密度泛函理论模拟进一步证明了S-Fe-抗生素电子转移途径，其中硫化物通过Fe(II)配位位点提供电子。使用天然河口沉积物进行的现场验证证实了实验室的发现，突出了黄铁矿介导的还原途径对抗生素衰减的重大贡献。这些发现推进了对河口环境中黄铁矿驱动的氧化还原过程的机制理解，并强调了硫物种在介导非自由基抗生素降解中被忽视的作用，对富硫沿海系统中的自然衰减和修复策略具有启示意义。
