Guangdong Provincial Key Laboratory of Petrochemical Pollution Processes and Control, School of Environmental Science and Engineering, Guangdong University of Petrochemical Technology Maoming, Guangdong 525000, China; College of Environmental Science and Engineering, Ocean University of China, Qingdao 266100, China.
Department of Civil and Environmental Engineering, The Hong Kong Polytechnic University, Hung Hom, Kowloon 999077, Hong Kong.
Ecotoxicol Environ Saf. 2024 Sep 15;283:116797. doi: 10.1016/j.ecoenv.2024.116797. Epub 2024 Jul 26.
Organophosphate esters (OPEs) are one of the emerging environmental threats, causing the hazard to ecosystem safety and human health. Yet, the toxic effects and metabolic response mechanism after Escherichia coli (E.coli) exposed to TDCIPP and TEHP is inconclusive. Herein, the levels of SOD and CAT were elevated in a concentration-dependent manner, accompanied with the increase of MDA contents, signifying the activation of antioxidant response and occurrence of lipid peroxidation. Oxidative damage mediated by excessive accumulation of ROS decreased membrane potential and inhibited membrane protein synthesis, causing membrane protein dysfunction. Integrative analyses of GC-MS and LC-MS based metabolomics evinced that significant perturbation to the carbohydrate metabolism, nucleotide metabolism, lipids metabolism, amino acid metabolism, organic acids metabolism were induced following exposure to TDCIPP and TEHP in E.coli, resulting in metabolic reprogramming. Additionally, metabolites including PE(16:1(5Z)/15:0), PA(17:0/15:1(9Z)), PC(20:2(11Z,14Z)/12:0), LysoPC(18:3(6Z,9Z,12Z)/0:0) were significantly upregulated, manifesting that cell membrane protective molecule was afforded by these differential metabolites to improve permeability and fluidity. Overall, current findings generate new insights into the molecular toxicity mechanism by which E.coli respond to TDCIPP and TEHP stress and supply valuable information for potential ecological risks of OPEs on aquatic ecosystems.
有机磷酸酯(OPEs)是一种新兴的环境威胁,对生态系统安全和人类健康造成危害。然而,大肠杆菌(E.coli)暴露于 TDCIPP 和 TEHP 后的毒性作用和代谢反应机制尚不清楚。本研究中,SOD 和 CAT 的水平呈浓度依赖性升高,同时 MDA 含量增加,表明抗氧化反应的激活和脂质过氧化的发生。过量 ROS 积累引起的氧化损伤降低了膜电位并抑制了膜蛋白合成,导致膜蛋白功能障碍。基于 GC-MS 和 LC-MS 的代谢组学综合分析表明,TDCIPP 和 TEHP 暴露后,大肠杆菌中的碳水化合物代谢、核苷酸代谢、脂质代谢、氨基酸代谢、有机酸代谢受到显著干扰,导致代谢重编程。此外,包括 PE(16:1(5Z)/15:0)、PA(17:0/15:1(9Z))、PC(20:2(11Z,14Z)/12:0)、LysoPC(18:3(6Z,9Z,12Z)/0:0)在内的代谢物显著上调,表明这些差异代谢物提供了细胞膜保护分子,以提高通透性和流动性。总之,本研究结果为大肠杆菌对 TDCIPP 和 TEHP 胁迫的分子毒性机制提供了新的见解,并为 OPEs 对水生生态系统的潜在生态风险提供了有价值的信息。