Wen Jingya, Liu Yajing, Xiao Botian, Zhang Zuning, Pu Qikun, Li Xixi, Ding Xiaowen, Qian Feng, Li Yu
College of Environmental Science and Engineering, North China Electric Power University, Beijing 102206, China.
State Environmental Protection Key Laboratory of Ecological Effect and Risk Assessment of Chemicals, National Engineering Laboratory for Lake Pollution Control and Ecological Restoration, Chinese Research Academy of Environmental Sciences, Beijing 100012, China; Northern Region Persistent Organic Pollution Control (NRPOP) Laboratory, Faculty of Engineering and Applied Science, Memorial University, St. John's, NL A1B 3x5, Canada.
J Hazard Mater. 2025 Mar 5;485:136888. doi: 10.1016/j.jhazmat.2024.136888. Epub 2024 Dec 15.
This study aimed to investigate the differences in the mechanisms of microscopic hepatotoxicity, developmental toxicity, and neurotoxicity in aquatic organisms co-exposed to styrene-butadiene rubber tire microplastics (SBR TMPs) and fluoroquinolone antibiotics (FQs). We found that hepatotoxicity in zebrafish induced by SBR TMPs and FQs was significantly higher than developmental toxicity and neurotoxicity. Furthermore, the main effects of the FQs primarily manifested as synergistic toxicity, whereas the low- and high-order interactions of the FQs mainly exhibited synergistic and antagonistic effects, respectively. Factorial analysis and the mixture toxicity index revealed that the synergistic effects of lomefloxacin × moxifloxacin and ciprofloxacin × lomefloxacin × enrofloxacin interactions significantly contributed to hepatotoxicity in zebrafish exposed to SBR TMP. SBR TMPs and antibiotics primarily induced hepatotoxicity, developmental toxicity, and neurotoxicity in zebrafish by affecting the activities of Cyp1a, Acox1, TRα, and mAChR. The observed toxicities were closely linked to the hydrophilic/hydrophobic groups, electronegativity, group mass, and structural complexity of the FQ molecules. This study provides new insights regarding the toxicological risks to aquatic organisms from co-exposure to SBR TMPs and FQs from a microscopic perspective. Future studies should include a broader range of antibiotics and tire microplastics and consider their long-term adverse effects on aquatic life.
本研究旨在探讨水生生物共同暴露于丁苯橡胶轮胎微塑料(SBR TMPs)和氟喹诺酮类抗生素(FQs)时,其微观肝毒性、发育毒性和神经毒性机制的差异。我们发现,SBR TMPs和FQs对斑马鱼诱导的肝毒性显著高于发育毒性和神经毒性。此外,FQs的主要作用主要表现为协同毒性,而FQs的低阶和高阶相互作用分别主要表现为协同和拮抗作用。因子分析和混合毒性指数表明,洛美沙星×莫西沙星以及环丙沙星×洛美沙星×恩诺沙星相互作用的协同效应显著导致了暴露于SBR TMP的斑马鱼的肝毒性。SBR TMPs和抗生素主要通过影响Cyp1a、Acox1、TRα和mAChR的活性,诱导斑马鱼的肝毒性、发育毒性和神经毒性。观察到的毒性与FQ分子的亲水/疏水基团、电负性、基团质量和结构复杂性密切相关。本研究从微观角度为共同暴露于SBR TMPs和FQs对水生生物的毒理学风险提供了新的见解。未来的研究应纳入更广泛的抗生素和轮胎微塑料,并考虑它们对水生生物的长期不利影响。