Plastics pose a hazard to the environment. Although plastics have toxicity, microplastics (MPs) and nanoplastics (NPs) are capable of interacting with the rest pollutants in the environment, so they serve as the carriers and interact with organic pollutants to modulate their toxicity, thus resulting in unpredictable ecological risks. PS-NPs and TDCIPP were used expose from 2 h post-fertilization (hpf) to 150 days post-fertilization (dpf) to determine the bioaccumulation of tris(1,3-dichloro-2-propyl) phosphate (TDCIPP) and its potential effects on neurodevelopment in F1 zebrafish (Danio rerio) offspring under the action of polystyrene nano plastics (PS-NPs). The exposure groups were assigned to TDCIPP (0, 0.4, 2 or 10 µg/L) alone group and the PS-NPs (100 µg/L) and TDCIPP co-exposed group. F1 embryos were collected and grown in clean water to 5 dpf post-fertilization. PS-NPs facilitated the bioaccumulation of TDCIPP in the gut, gill, head，gonad and liver of zebrafish in a sex-dependent manner and promoted the transfer of TDCIPP to their offspring, thus contributing to PS-NPs aggravated the inhibition of offspring development and neurobehavior of TDCIPP-induced. In comparison with TDCIPP exposure alone, the combination could notably down-regulate the levels of the dopamine neurotransmitter, whereas the levels of serotonin or acetylcholine were not notably different. This result was achieved probably because PS-NPs interfered with the TDCIPP neurotoxic response of zebrafish F1 offspring not through the serotonin or acetylcholine neurotransmitter pathway. The increased transfer of TDCIPP to the offspring under the action of PS-NPs increased TDCIPP-induced transgenerational developmental neurotoxicity, which was proven by a further up-regulation/down-regulation the key gene and protein expression related to dopamine synthesis, transport, and metabolism in F1 larvae, in contrast to TDCIPP exposure alone. The above findings suggested that dopaminergic signaling involvement could be conducive to the transgenerational neurodevelopmental toxicity of F1 larval upon parental early co-exposure to PS-NPs and TDCIPP.

中文翻译：

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纳米塑料根据多巴胺信号通路的参与加剧了 TDCIPP 诱导的斑马鱼跨代发育神经毒性

塑料对环境造成危害。塑料虽然具有毒性，但微塑料（MP）和纳米塑料（NP）能够与环境中的其他污染物相互作用，因此它们作为载体与有机污染物相互作用调节其毒性，从而产生不可预测的生态风险。使用 PS-NP 和 TDCIPP 从受精后 2 小时 (hpf) 到受精后 150 天 (dpf) 进行暴露，以确定磷酸三(1,3-二氯-2-丙基)酯 (TDCIPP) 的生物累积性及其潜力聚苯乙烯纳米塑料 (PS-NP) 作用下对 F1 斑马鱼 (Danio rerio) 后代神经发育的影响。暴露组被分配为单独TDCIPP（0、0.4、2或10μg/L）组和PS-NPs（100μg/L）和TDCIPP共同暴露组。收集 F1 胚胎并在干净的水中生长至受精后 5 dpf。 PS-NPs以性别依赖性方式促进TDCIPP在斑马鱼肠道、鳃、头部、性腺和肝脏中的生物积累，并促进TDCIPP向后代的转移，从而导致PS-NPs加剧对后代发育的抑制， TDCIPP 诱导的神经行为。与单独暴露于 TDCIPP 相比，该组合可以显着下调多巴胺神经递质的水平，而血清素或乙酰胆碱的水平没有显着差异。这一结果的实现可能是因为 PS-NPs 不是通过血清素或乙酰胆碱神经递质途径干扰斑马鱼 F1 后代的 TDCIPP 神经毒性反应。在 PS-NP 的作用下，TDCIPP 向后代的转移增加，增加了 TDCIPP 诱导的跨代发育神经毒性，这通过进一步上调/下调与多巴胺合成、运输和代谢相关的关键基因和蛋白质表达来证明。 F1 幼虫的代谢，与单独暴露于 TDCIPP 相比。上述研究结果表明，多巴胺能信号传导参与可能有助于 F1 幼虫在亲代早期同时接触 PS-NP 和 TDCIPP 时产生跨代神经发育毒性。