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从接口到细胞:微塑料和抗生素耐药性基因之间的复杂相互作用和转移过程合机制

Hongyu Tian^1,2, Jianwei Liu^1,3, Lin Li^4,5

¹Key Laboratory of Urban Stormwater System and Water Environment, Beijing University of Civil Engineering and Architecture, Ministry of Education, Beijing 100044, China.

Environmental science & technology

|February 1, 2026

概括

微塑料通过改变废水处理接口,促进细菌粘附,并通过氧化和膜相互作用增加基因转移来加速抗生素耐药性基因的传播. 这突显了微塑料污染是传播抗生素耐药性的关键因素.

科学领域:

环境科学环境科学
微生物学微生物学
材料科学材料科学材料科学

背景情况:

微塑料相接口 (MPPI) 正在成为抗生素耐药性基因 (ARG) 传播的重要载体.
了解MP-ARG相互作用的机制对于减轻环境风险至关重要.

研究的目的:

阐明废水处理系统中的界面和细胞尺度上的微塑料 (MP) 和ARG之间的相互作用机制.
调查MP老化和材料类型对ARG传播的影响.

主要方法:

综合无氧/有氧废水处理实验.
老年国会议员的物理化学特征.
对于ARG和移动遗传元素 (MGE) 分析的元基因组测序.
分子动力学 (MD) 模拟和XDLVO理论用于相互作用分析.

主要成果:

聚合物聚合物的老化 (PET,PE,PP) 导致表面转化 (元素丰富,功能组,氧化),增强了细胞外聚合物物质的产生.
选择性丰富MPPI抗生素耐药细菌,ARG和MGE,促进横向基因转移.
MD模拟显示了由Lifshitz-van der Waals力驱动的直接MP膜透和透率的增加.
MPPI诱导了反应性氧物种 (ROS) 的过度生产,对参与排泄,毛孔和结合性转移的关键基因进行了上调.

结论:

MP老化和表面特性显著影响废水处理中的ARG传播.
物理相互作用 (粘附,透) 和氧化应激都会导致ARG的丰富和转移.
有氧条件有利于基因驱动的氧化和MGE捕获,而无氧条件增强了疏水性粘附,表明了特定于材料和依赖氧气的机制.

关键词:

无氧/有氧废水处理系统.抗生素耐药性基因是抗生素耐药性的基因.交互和转移过程合机制的机制.微塑料微塑料的使用阶段界面的相位界面接口.

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