Plastic is a globally recognized superwaste that can affect human health and wildlife when it accumulates and is amplified in the food chain. Microplastics (plastic particles < 5 mm) and nanoplastics (plastic particles < 100 nm) can interact with organic pollutants already present in the aquatic environment, potentially acting as carriers for pollutants entering organisms and thus influencing the bioavailability and toxicity of those pollutants. In this study, we investigated the transfer kinetics and transgenerational effects of exposure to tris(1,3-dichloro-2-propyl) phosphate (TDCIPP) and polystyrene nanoplastics (PS-NPs) in F1 offspring. At 90 days postfertilization, zebrafish (Danio rerio) strain AB was exposed to either TDCIPP (0, 0.47, 2.64, or 12.78 μg/L) or PS-NPs (10 mg/L) or their combination for 120 days. The results showed that TDCIPP and PS-NPs accumulated in the gut, gill, head, and liver of the zebrafish in a sex-dependent manner. The presence of PS-NPs promoted the bioaccumulation of TDCIPP in the adult fish and increased the parental transfer of TDCIPP to their offspring. We demonstrate that parental exposure to TDCIPP alone or in combination with PS-NPs induces thyroid disruption in adults, and then leads to thyroid endocrine disruption in their larval offspring. Reduced thyroxine (T4) and 3,5,3′-triiodothyronine (T3) levels contributed to the observed transgenerational thyroid dysfunction, which inhibited developmental growth and disturbed the transcription of genes and expression of proteins involved in the hypothalamic–pituitary–thyroid (HPT) axis in the F1 larvae. The increased transfer of TDCIPP to the offspring in the presence of PS-NPs also enhanced transgenerational thyroid endocrine disruption, demonstrated by a further reduction in T4 and the upregulation of thyroglobulin (tg), uridine diphosphate-glucuronosyltransferase (ugt1ab), thyroid-stimulating hormone (tshβ), and thyroid hormone receptor (trα) expression in the F1 larvae compared with the effects of parental TDCIPP exposure alone. Overall, our results indicate that the presence of PS-NPs modifies the bioavailability of TDCIPP and aggravates transgenerational thyroid disruption in zebrafish.

塑料是一种全球公认的超级废物，当它在食物链中积累和放大时，会影响人类健康和野生动物。微塑料（塑料颗粒 < 5 毫米）和纳米塑料（塑料颗粒 < 100 纳米）可以与水生环境中已经存在的有机污染物相互作用，可能作为污染物进入生物体的载体，从而影响这些污染物的生物利用度和毒性。在这项研究中，我们研究了 F1 后代暴露于三（1,3-二氯-2-丙基）磷酸酯 (TDCIPP) 和聚苯乙烯纳米塑料 (PS-NPs) 的转移动力学和跨代效应。在受精后 90 天，斑马鱼 ( Danio rerio) 菌株 AB 暴露于 TDCIPP（0、0.47、2.64 或 12.78 μg/L）或 PS-NPs（10 mg/L）或它们的组合中 120 天。结果表明，TDCIPP 和 PS-NPs 以性别依赖性方式在斑马鱼的肠道、鳃、头部和肝脏中积累。PS-NPs 的存在促进了 TDCIPP 在成年鱼中的生物积累，并增加了 TDCIPP 向其后代的亲本转移。我们证明，父母单独接触 TDCIPP 或与 PS-NP 联合使用会诱导成虫的甲状腺功能紊乱，然后导致其幼虫后代的甲状腺内分泌紊乱。甲状腺素 (T4) 和 3,5,3'-三碘甲状腺原氨酸 (T3) 水平降低导致观察到的跨代甲状腺功能障碍，这抑制了发育生长并扰乱了 F1 幼虫中涉及下丘脑-垂体-甲状腺 (HPT) 轴的基因转录和蛋白质表达。在 PS-NPs 存在的情况下，TDCIPP 向后代转移的增加也增强了跨代甲状腺内分泌紊乱，这可以通过 T4 的进一步降低和甲状腺球蛋白的上调来证明。tg )、尿苷二磷酸-葡萄糖醛酸转移酶 ( ugt1ab )、促甲状腺激素 ( tshβ ) 和甲状腺激素受体 ( trα ) 在 F1 幼虫中的表达与亲本 TDCIPP 单独暴露的影响相比。总的来说，我们的结果表明 PS-NPs 的存在改变了 TDCIPP 的生物利用度，并加剧了斑马鱼的跨代甲状腺破坏。