Abstract：
Microplastic pollution poses challenges for ecosystems worldwide, and nanoplastics (NPs, 1-1000 nm) have been identified as persistent pollutants. However, although some studies have described the hazards of NPs to aquatic organisms, the toxicological processes of NPs in the common carp kidney and the biotoxicity of differently sized NPs remain unclear. In this study, we used juvenile common carp as an in vivo model that were constantly exposed to freshwater at 1000 μg/L polystyrene nanoparticle (PSNP) concentrations (50, 100, and 400 nm) for 28 days. Simultaneously, we constructed an in vitro model utilizing grass fish kidney cells (CIK) to study the toxicological effects of PSNPs of various sizes. We performed RT-PCR and Western blot assays on the genes involved in FOXO1, HMGB1, HIF-1α, endoplasmic reticulum stress, autophagy, and immunoreaction. According to these results, exposure to PSNPs increased reactive oxygen species (ROS) levels, and the carp kidneys experienced endoplasmic reticulum stress. Additionally, PSNPs promoted renal autophagy by activating the ROS/ERS/FOXO1 (ERS: endoplasmic reticulum stress) pathway, and it affected immunological function by stimulating the ROS/HMGB1/HIF-1α signaling pathway. This study provides new insights into the contamination hazards of NPs in freshwater environments, as well as the harm they pose to the human living environments. The relationship between particle size and the degree of damage caused by PSNPs to organisms is a potential future research direction.
摘要：
微塑料污染对全球生态系统构成挑战，和纳米塑料(NPs，1-1000nm）已被确定为持久性污染物。然而,尽管一些研究已经描述了NP对水生生物的危害，NPs在鲤鱼肾脏中的毒理学过程和不同大小NPs的生物毒性仍不清楚。在这项研究中,我们使用幼鱼作为体内模型,在1000μg/L聚苯乙烯纳米颗粒(PSNP)浓度(50,100和400nm)的淡水中持续暴露28天.同时,我们利用草鱼肾细胞（CIK）构建了体外模型，以研究各种大小的PSNP的毒理学作用。我们对FOXO1、HMGB1、HIF-1α、内质网应激,自噬,和免疫反应。根据这些结果,暴露于PSNP会增加活性氧（ROS）水平，鲤鱼肾脏经历了内质网应激。此外,PSNPs通过激活ROS/ERS/FOXO1（ERS：内质网应激）途径促进肾脏自噬，并通过刺激ROS/HMGB1/HIF-1α信号通路影响免疫功能。这项研究为淡水环境中NP的污染危害提供了新的见解，以及它们对人类生存环境的危害。颗粒大小与PSNPs对生物体的损伤程度之间的关系是一个潜在的未来研究方向。
