Understanding the role of microplastics (MPs) in the biological fate and toxicity of organic pollutants in food webs is vital for its risk assessment. However, contradictory results and the neglect of MP aging as a factor have led to a research gap, which needs to be filled. Our study discovered that polyamide (PA, a ubiquitous MP in water) MPs clearly facilitated bioaccumulation of tris(1,3-dichloro-2-propyl) phosphate (TDCIPP) in the F0 zebrafish gonads and parental transfer of TDCIPP to the F1 offspring. Rapid TDCIPP desorption in the gut and intestine barrier dysfunction triggered by MPs were the causes for the phenomenon. In contrast to the pristine forms, aged PA with higher hydrophilcity exhibited stronger binding and polar interactions with TDCIPP, and the intestine damage was neglectable, resulting in increased intestinal immobilization and prevented parental transfer of TDCIPP. Additionally, the aggravated body weight loss and decreased length of TDCIPP offspring were relieved after PA aging. The recovery of subintestinal venous plexus angiogenesis, yolk lipid utilization, and ATP synthesis were responsible for the mitigated transgenerational toxicity. Our results highlight the significance of aging on the role of MPs with respect to coexisting pollutants and have great implications for understanding MP-associated risks.

了解微塑料 (MPs) 在食物网中有机污染物的生物归宿和毒性中的作用对于其风险评估至关重要。然而，相互矛盾的结果以及对 MP 老化这一因素的忽视导致了一个需要填补的研究空白。我们的研究发现，聚酰胺（PA，一种普遍存在于水中的 MP）MPs 明显促进了 F0 斑马鱼性腺中三（1,3-二氯-2-丙基）磷酸盐 (TDCIPP) 的生物积累和 TDCIPP 向 F1 后代的亲代转移。由 MP 引发的肠道中 TDCIPP 的快速解吸和肠道屏障功能障碍是该现象的原因。与原始形式相比，具有更高亲水性的老化PA与TDCIPP表现出更强的结合和极性相互作用，并且肠道损伤可以忽略不计，导致肠道固定增加并阻止 TDCIPP 的亲本转移。此外，PA老化后TDCIPP后代体重减轻加重和身长缩短得到缓解。肠下静脉丛血管生成、卵黄脂质利用和 ATP 合成的恢复是减轻跨代毒性的原因。我们的研究结果强调了老龄化对 MP 在共存污染物方面的作用的重要性，并对理解 MP 相关风险具有重要意义。和 ATP 合成是减轻跨代毒性的原因。我们的研究结果强调了老龄化对 MP 在共存污染物方面的作用的重要性，并对理解 MP 相关风险具有重要意义。和 ATP 合成是减轻跨代毒性的原因。我们的研究结果强调了老龄化对 MP 在共存污染物方面的作用的重要性，并对理解 MP 相关风险具有重要意义。