Here, we subjected the marine copepod to environmentally-relevant concentrations of microplastics (MPs) and mercury (Hg) for three generations (F0–F2) to investigate their physiological and molecular responses. Hg accumulation and phenotypic traits were measured in each generation, with multi-omics analysis conducted in F2. The results showed that MPs insignificantly impacted the copepod’s development and reproduction, however, which were significantly compromised by Hg exposure. Interestingly, MPs significantly increased Hg accumulation and consequently aggravated this metal toxicity in , demonstrating their carrier role. Multi-omics analysis indicated that Hg pollution produced numerous toxic events, e.g., induction of apoptosis, damage to cell/organ morphogenesis, and disordered energy metabolism, ultimately resulting in retarded development and decreased fecundity. Importantly, MPs enhanced Hg toxicity mainly via increased oxidative apoptosis, compromised cell/organ morphogenesis, and energy depletion. Additionally, phosphoproteomic analysis revealed extensive regulation of the above processes, and also impaired neuron activity under combined MPs and Hg exposure. These alterations adversely affected development and reproduction of . Overall, our findings should offer novel molecular insights into the response of to long-term exposure to MPs and Hg, with a particular emphasis on the carrier role of MPs on Hg toxicity.

中文翻译：

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环境相关剂量的微塑料会增强多代暴露下海洋桡足类的汞毒性：多组学视角


在这里，我们将海洋桡足类动物置于环境相关浓度的微塑料 (MP) 和汞 (Hg) 环境中三代 (F0-F2)，以研究它们的生理和分子反应。测量每一代的汞积累和表型性状，并在 F2 中进行多组学分析。结果表明，MP 对桡足类的发育和繁殖影响不大，但汞暴露却严重影响了它们的发育和繁殖。有趣的是，MP 显着增加了汞的积累，从而加剧了这种金属毒性，证明了它们的载体作用。多组学分析表明，汞污染会产生多种毒性事件，如诱导细胞凋亡、细胞/器官形态发生受损、能量代谢紊乱等，最终导致发育迟缓和繁殖力下降。重要的是，MP 主要通过增加氧化凋亡、损害细胞/器官形态发生和能量消耗来增强汞毒性。此外，磷酸化蛋白质组学分析揭示了上述过程的广泛调节，并且在 MP 和 Hg 联合暴露下神经元活动也受损。这些改变对 的发育和繁殖产生了不利影响。总的来说，我们的研究结果应该为长期接触 MP 和 Hg 的反应提供新的分子见解，特别强调 MP 对汞毒性的载体作用。