Plastics are world-wide pollutants that pose a potential threat to wildlife and human health. Small plastic particles, such as microplastics and nanoplastics, are easily ingested, and can act as a Trojan Horse by carrying microorganisms and pollutants. This study investigated the potential role of the Trojan Horse effect in the toxicity of nanoplastics to the vertebrate model organism, zebrafish (Danio rerio). First, we investigated if this effect could affect the toxicity of nanoplastics. Second, we analyzed if it could contribute to the biodistribution of the associated contaminants. And third, we focused on its effect on the mitochondrial toxicity of nanoplastics. We incubated 44 nm polystyrene nanoparticles with a real-world mixture of polycyclic aromatic hydrocarbons (PAHs) for 7 days and removed the free PAHs by ultrafiltration. We dosed embryos with 1 ppm of nanoplastics (NanoPS) or PAH-sorbed nanoplastics (PAH-NanoPS). Neither type of plastic particle caused changes in embryonic and larval development. Fluorescence microscopy and increased EROD activity suggested the uptake of PAHs in larvae exposed to PAH-NanoPS. This coincided with higher concentrations in the yolk sac and the brain. However, PAH-only exposure leads to their accumulation in the yolk sac but not in the brain, suggesting that that the spatial distribution of bioaccumulated PAHs can differ depending on their source of exposure. Both nanoplastic particles affected mitochondrial energy metabolism but caused different adverse effects. While NanoPS decreased NADH production, PAH-NanoPS decreased mitochondrial coupling efficiency and spare respiratory capacity. In summary, the addition of PAHs to the surface of nanoplastics did not translate into increased developmental toxicity. Low levels of PAHs were accumulated in the organisms, and the transfer of PAHs seems to happen in tissues and possibly organelles where nanoplastics accumulate. Disruption of the energy metabolism in the mitochondria may be a key factor in the toxicity of nanoplastics, and the Trojan Horse effect may amplify this effect.

中文翻译：

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PAH 对纳米塑料的吸附和特洛伊木马效应是斑马鱼线粒体毒性和 PAH 定位的驱动因素

塑料是世界范围内的污染物，对野生动物和人类健康构成潜在威胁。小的塑料颗粒，如微塑料和纳米塑料，很容易被摄入，并且可以通过携带微生物和污染物来充当特洛伊木马。本研究调查了特洛伊木马效应在纳米塑料对脊椎动物模式生物斑马鱼 (Danio rerio) 的毒性中的潜在作用。首先，我们研究了这种效应是否会影响纳米塑料的毒性。其次，我们分析了它是否有助于相关污染物的生物分布。第三，我们关注其对纳米塑料线粒体毒性的影响。我们将 44 nm 聚苯乙烯纳米粒子与真实世界的多环芳烃 (PAH) 混合物孵育 7 天，并通过超滤去除游离的 PAH。我们给胚胎注射了 1 ppm 的纳米塑料 (NanoPS) 或吸附多环芳烃的纳米塑料 (PAH-NanoPS)。这两种塑料颗粒都不会引起胚胎和幼虫发育的变化。荧光显微镜和增加的 EROD 活性表明暴露于 PAH-NanoPS 的幼虫吸收了 PAH。这与卵黄囊和大脑中较高的浓度相吻合。然而，仅暴露于多环芳烃会导致它们在卵黄囊中而不是在大脑中积累，这表明生物积累的多环芳烃的空间分布可能因它们的暴露来源而异。两种纳米塑料颗粒都会影响线粒体能量代谢，但会产生不同的副作用。NanoPS 会降低 NADH 的产生，而 PAH-NanoPS 会降低线粒体耦合效率和备用呼吸能力。总之，在纳米塑料表面添加多环芳烃并没有转化为增加的发育毒性。生物体中积累了低水平的多环芳烃，多环芳烃的转移似乎发生在纳米塑料积累的组织和可能的细胞器中。线粒体中能量代谢的中断可能是纳米塑料毒性的关键因素，而特洛伊木马效应可能会放大这种效应。