近年來，全球塑膠使用量與工業排放量持續攀升，使微/奈米塑膠(MP/NPs)與重金屬成為水域生態中最具代表性的複合型污染物，塑膠在經紫外線、機械磨損與化學老化過程逐漸降解成微/奈米尺寸，其粒徑極小、表面積高、可穿透生物屏障，更可能吸附環境中其他污染物，使其毒性大幅改變；而重金屬如六價鉻（Cr⁶⁺）與銅離子（Cu²⁺）廣泛來源於電鍍、電子製造等工業活動，不僅難以降解，亦具高度的急毒性及生物累積性，多篇研究指出奈米塑膠可能作為污染物載體，促使重金屬以更高效率進入水生生物體內，導致混合暴露之毒性遠高於單一污染物，然而現階段針對奈米塑膠與重金屬共同暴露在水生生物早期發育，尤其是魚鰾發育過程中的影響仍所知有限，因此深入理解奈米塑膠如何改變重金屬在胚胎中的毒性與作用機制，對於生態風險評估與環境監測策略具有重要意義。
本研究依據OECD TG 236進行斑馬魚胚胎急毒性測試，評估PS NPs與K2Cr2O7、CuSO4·5H2O溶液共同暴露對胚胎早期發育之影響，將受精後的胚胎分別進行金屬單獨暴露以及共同暴露PS NPs 96小時，並評估死亡率、孵化率、體長、心率及畸形等發育端點，此外以DCFH-DA分析ROS生成量，並以 ICP-MS 測量胚胎內金屬累積，並評估兩者間是否存在協同作用，接著進一步針對魚鰾發育進行觀察，包括魚鰾缺失率、魚鰾尺寸、游泳行為及魚鰾發育相關基因表達。
研究結果顯示，PS-NPs單獨暴露對胚胎影響有限，但與Cr⁶⁺或Cu²⁺共同暴露時，胚胎死亡率明顯上升，孵化率降低與體長、心率異常更為顯著，且多重畸形發生比例大幅增加，特別是魚鰾未充氣現象，共同暴露組的魚鰾缺失率顯著增加，魚鰾尺寸明顯縮小，且游泳距離與活動時間下降，基因表達量顯著下調，反映魚鰾功能已受到破壞；PS-NPs會使Cr⁶⁺與Cu²⁺在胚胎內累積量增加，證實PS NPs具提升重金屬生物可利用性的能力；同時發現共同暴露PS NPs後會使胚胎內的的ROS含量提高；最後協同作用分析證實PS-NPs與兩種重金屬之間存在明顯的協同作用。
本研究證實奈米聚苯乙烯能顯著放大重金屬對斑馬魚胚胎的毒性，特別是在魚鰾這一高度敏感器官上表現最為明顯，說明魚鰾可作為評估奈米塑膠和重金屬交互作用的重要生物指標，並為未來水生環境中的混合污染風險評估提供重要科學基礎。

Micro- and nanoplastics (MPs/NPs) and heavy metals have emerged as major co-occurring contaminants in aquatic environments due to increasing plastic usage and industrial discharge. Plastics progressively fragment into nanoscale particles with the ability to cross biological barriers, allowing them to adsorb pollutants and potentially alter their toxicity. Heavy metals such as hexavalent chromium (Cr⁶⁺) and copper ions (Cu²⁺), widely released from electroplating and electronics manufacturing, are highly toxic and bioaccumulative. In this study, zebrafish embryos were exposed for 96 hours to PS-NPs, K₂Cr₂O₇, CuSO₄·5H₂O, or their mixtures following OECD TG 236. Developmental endpoints including mortality, hatching, body length, heart rate, and deformations were assessed, ROS levels and metal accumulation were analyzed to investigate underlying mechanisms and potential synergistic toxicity, and swim bladder development was examined through uninflated rate, size, behavior, and gene expression.
The results showed that while PS-NPs alone induced minimal effects, co-exposure with Cr⁶⁺ or Cu²⁺ increased mortality, delayed hatching, impaired growth, altered cardiac function, and intensified malformations.Mechanistic analyses revealed increased metal accumulation and elevated ROS, suggesting enhanced metal bioavailability. Swim bladder defects were the most prominent, with higher uninflated rates, reduced size, decreased swimming activity, and downregulated developmental genes.These findings demonstrate that PS-NPs amplify heavy metal toxicity in embryos and highlight the swim bladder as a sensitive biomarker for assessing mixed-pollution risks in aquatic environments.

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