Zhuang Ziyi, Wang Yifan, Zhang Zhourui, Zhang Weiwei, Ding Jieyu, Weng Zufeng, Chen Xinhua, Hu Fengxiao
Key Laboratory of Marine Biotechnology of Fujian Province, College of Marine Sciences, Fujian Agriculture and Forestry University, Fuzhou 350002, PR China.
Pingtan Comprehensive Experimental Zone Marine and Fisheries Law Enforcement Detachment, Pingtan 350400, PR China.
J Hazard Mater. 2025 Sep 15;496:139337. doi: 10.1016/j.jhazmat.2025.139337. Epub 2025 Jul 22.
The occurrence of tire-derived chemical N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine quinone (6PPD-Q) has raised concerns about its environmental toxicity. However, the toxicity of 6PPD-Q on aquatic invertebrates remains insufficiently characterized. In this study, a model organism, Daphnia magna, was exposed to 0, 0.2, 2, and 20 μg/L 6PPD-Q for 21 days to assess the potential effects of 6PPD-Q on its growth, reproduction, and antioxidant defense. The results showed that long-term exposure to 6PPD-Q led to a pronounced reduction in the body length of D. magna, which was associated with disturbance of the ecdysteroid signaling pathway. 6PPD-Q was proven to be an antagonist of 20-Hydroxyecdysone (20-HE) through a dual-luciferase reporter assay, competitively binding to the heterodimer composed of ecdysone receptor (EcR) and ultraspiracle (USP), and ultimately interfering with the expression of downstream genes. 6PPD-Q markedly delayed the time to first brood and diminished the number of neonates per adult, the average number of neonates per time as well as spawning times. The declined expressions of reproduction-related genes vtg1, vtg2, and vmo1, regulated by an elevated juvenile hormone (JH) level, might account for the reduced fecundity of D. magna. In addition, 6PPD-Q activated the antioxidant defense of D. magna, enabling it to remove excessive ROS and prevent lipid oxidative damage. Collectively, a trade-off between growth, reproduction, and antioxidant defense was suggested in D. magna under 6PPD-Q stress. Our findings provide valuable information for the risk assessment of 6PPD-Q to the freshwater ecosystem.
轮胎衍生化学物质N-(1,3-二甲基丁基)-N'-苯基-对苯二胺醌(6PPD-Q)的出现引发了人们对其环境毒性的担忧。然而,6PPD-Q对水生无脊椎动物的毒性仍未得到充分表征。在本研究中,模式生物大型溞暴露于0、0.2、2和20μg/L的6PPD-Q中21天,以评估6PPD-Q对其生长、繁殖和抗氧化防御的潜在影响。结果表明,长期暴露于6PPD-Q会导致大型溞体长显著缩短,这与蜕皮类固醇信号通路的紊乱有关。通过双荧光素酶报告基因检测,证明6PPD-Q是20-羟基蜕皮酮(20-HE)的拮抗剂,它竞争性地与由蜕皮激素受体(EcR)和超气门蛋白(USP)组成的异二聚体结合,最终干扰下游基因的表达。6PPD-Q显著延迟了首次产卵的时间,减少了每只成年个体的幼体数量、每次的平均幼体数量以及产卵次数。由升高的保幼激素(JH)水平调节的生殖相关基因vtg1、vtg2和vmo1表达下降,可能是大型溞繁殖力降低的原因。此外,6PPD-Q激活了大型溞的抗氧化防御系统,使其能够清除过量的活性氧并防止脂质氧化损伤。总体而言,在6PPD-Q胁迫下,大型溞在生长、繁殖和抗氧化防御之间存在权衡。我们的研究结果为评估6PPD-Q对淡水生态系统的风险提供了有价值的信息。