Nanopolystyrene (NPS), a frequently employed nanoplastic, is an emerging environmental contaminant known to cause neurotoxicity in various organisms. However, the potential for transgenerational neurotoxic effects, especially from photoaged NPS (P-NPS), remains underexplored. This study investigated the aging of virgin NPS (V-NPS) under a xenon lamp to simulate natural sunlight exposure, which altered the physicochemical characteristics of the NPS. The parental generation (P0) of Caenorhabditis elegans was exposed to environmental concentrations (0.1–100 μg/L) of V-NPS and P-NPS, with subsequent offspring (F1–F4 generations) cultured under NPS-free conditions. Exposure to 100 μg/L P-NPS resulted in more pronounced deterioration in locomotion behavior in the P0 generation compared to V-NPS; this deterioration persisted into the F1–F2 generations but returned to normal in the F3–F4 generations. Additionally, maternal exposure to P-NPS damaged dopaminergic, glutamatergic, and serotonergic neurons in subsequent generations. Correspondingly, there was a significant decrease in the levels of dopamine, glutamate, and serotonin, associated with reduced expression of neurotransmission-related genes dat-1, eat-4, and tph-1 in the P0 and F1–F2 generations. Further analysis showed that the effects of P-NPS on locomotion behavior were absent in subsequent generations of eat-4(ad572), tph-1(mg280), and dat-1(ok157) mutants, highlighting the pivotal roles of these genes in mediating P-NPS-induced transgenerational neurotoxicity. These findings emphasize the crucial role of neurotransmission in the transgenerational effects of P-NPS on locomotion behavior, providing new insights into the environmental risks associated with exposure to photoaged nanoplastics.

中文翻译：

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光老化纳米聚苯乙烯影响神经传递以诱导秀丽隐杆线虫的跨代神经毒性


纳米聚苯乙烯（NPS）是一种常用的纳米塑料，是一种新兴的环境污染物，已知会导致多种生物体的神经毒性。然而，跨代神经毒性作用的潜力，尤其是光老化 NPS (P-NPS) 的潜力，仍未得到充分探索。本研究研究了原始 NPS (V-NPS) 在氙灯下模拟自然阳光照射的老化情况，这改变了 NPS 的物理化学特性。线虫亲代 (P0) 暴露于环境浓度 (0.1–100 μg/L) 的 V-NPS 和 P-NPS，随后的后代（F1–F4 代）在无 NPS 的条件下培养。与 V-NPS 相比，暴露于 100 μg/L P-NPS 会导致 P0 代的运动行为更加明显恶化；这种恶化持续到 F1-F2 代，但在 F3-F4 代中恢复正常。此外，母亲接触 P-NPS 会损害后代的多巴胺能、谷氨酸能和血清素能神经元。相应地，在 P0 和 F1-F2 代中，多巴胺、谷氨酸和血清素水平显着下降，这与神经传递相关基因 dat-1、eat-4 和 tph-1 的表达减少有关。进一步分析表明，P-NPS 对运动行为的影响在 eat-4(ad572)、tph-1(mg280) 和 dat-1(ok157) 突变体的后代中不存在，突出了这些基因在运动中的关键作用。介导 P-NPS 诱导的跨代神经毒性。这些发现强调了神经传递在 P-NPS 对运动行为的跨代影响中的关键作用，为与暴露于光老化纳米塑料相关的环境风险提供了新的见解。