Mei Mengyuan, Deng Lin, Lin Zihan, Ai Fuxun, Yin Ying, Guo Hongyan
State Key Laboratory of Water Pollution Control and Green Resource Recycling, School of the Environment, Nanjing University, Nanjing 210023, China.
State Key Laboratory of Water Pollution Control and Green Resource Recycling, School of the Environment, Nanjing University, Nanjing 210023, China; Joint International Research Centre for Critical Zone Science-University of Leeds and Nanjing University, Nanjing University, Nanjing 210023, China.
J Hazard Mater. 2025 Sep 15;496:139238. doi: 10.1016/j.jhazmat.2025.139238. Epub 2025 Jul 13.
As a representative organophosphate flame retardant (OPFR), triphenyl phosphate (TPHP) is ubiquitously detected in aquatic environments. The aquatic ecotoxicity of TPHP is mostly focused on fish, with fewer studies on microalgae, a key producer that affects the aquatic ecological balance. This study systematically deciphered the dose-dependent effects of TPHP (0.1-2 mg/L) on Microcystis aeruginosa (M. aeruginosa) through integrated physiological assays, stable isotope (C) test, transcriptomics, and microcystin-LR (MC-LR) profiling. The concentration distribution analysis demonstrated strong algal-mediated TPHP degradation (26-63 % degradation), with 28-35 % of the residual TPHP adsorbed on cell surfaces and 30-51 % accumulated intracellularly. While inducing concentration-dependent membrane alterations, TPHP exposure maintained algal growth and photosynthetic competence. Notably, at elevated concentrations (1-2 mg/L), TPHP enhanced photosynthetic performance and biomass production through coordinated upregulation of core metabolic pathways encompassing photosynthesis, carbon metabolism, oxidative phosphorylation, and protein biosynthesis. Concurrently, M. aeruginosa activated multiple defense mechanisms against TPHP stress, characterized by extracellular protein overproduction, tryptophan enrichment in extracellular polymeric substances, and intensified MC-LR synthesis/release. These findings reveal a dual role of TPHP as both a metabolic stimulant and toxic stressor, potentially reshaping algal community dynamics and exacerbating harmful algal bloom risks. This work provides critical mechanistic insights for refining OPFR risk assessment protocols in aquatic systems.
作为一种典型的有机磷酸酯阻燃剂(OPFR),磷酸三苯酯(TPHP)在水生环境中广泛存在。TPHP的水生生态毒性研究主要集中在鱼类,而对作为影响水生生态平衡关键生产者的微藻的研究较少。本研究通过综合生理测定、稳定同位素(C)测试、转录组学和微囊藻毒素-LR(MC-LR)分析,系统地解析了TPHP(0.1-2 mg/L)对铜绿微囊藻(M. aeruginosa)的剂量依赖性影响。浓度分布分析表明,藻类对TPHP有较强的降解作用(降解率为26-63%),28-35%的残留TPHP吸附在细胞表面,30-51%在细胞内积累。TPHP暴露在诱导浓度依赖性膜改变的同时,维持了藻类的生长和光合能力。值得注意的是,在较高浓度(1-2 mg/L)下,TPHP通过协同上调包括光合作用、碳代谢、氧化磷酸化和蛋白质生物合成在内的核心代谢途径,增强了光合性能和生物量生产。同时,铜绿微囊藻激活了多种针对TPHP胁迫的防御机制,其特征是细胞外蛋白质过量产生、细胞外聚合物中色氨酸富集以及MC-LR合成/释放增强。这些发现揭示了TPHP作为代谢刺激物和毒性应激源的双重作用,可能重塑藻类群落动态并加剧有害藻华风险。这项工作为完善水生系统中OPFR风险评估方案提供了关键的机制性见解。