Significant concerns have been raised by the widespread pollutants phoxim (PHO) and nanopolystyrene (NP) in the natural environment. This study evaluated the toxicity effects on the hepatopancreas of Eriocheir sinensis caused by NP and/or PHO at concentrations found in the environment. Subchronic exposure to NP and/or PHO triggered hepatopancreas histological damage within a 21-day exposure period. The NP, PHO, and co-exposure (NPO) groups exhibited fewer blister-like (B) cells, along with the appearance of vacuolation. Furthermore, these exposures induced impairment in the hepatic tubule mucus barrier and mechanical barrier, as evidenced by altered expression of oxidative stress-related genes, mucin-related genes, and TJ-related genes. Additionally, alterations in immunity-related genes and inflammatory cytokine genes expression were observed. The findings showed that hepatopancreas inflammation was caused by both individual and combined exposure to NP and PHO and that the inflammatory response was exacerbated by the co-exposure. The possible pathways of hepatopancreas toxicity were further investigated by transcriptomic analysis. Hepatopancreas inflammation was brought on by subchronic exposure to PHO and co-exposure; this inflammation was exacerbated by co-exposure and was backed by the activation of NF-κB signaling pathway via targeting-related genes. In summary, this research represents the initial documentation, to the best of our understanding of the detrimental effects of exposured to NP and/or PHO at levels found in the environment disrupt the hepatopancreas mucus and mechanical barrier in crustaceans, triggering inflammatory responses. These findings highlight the significance of NP and/or PHO pollution for hepatopancreas health.

中文翻译：

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纳米聚苯乙烯和磷氧污染：对中华绒螯蟹 （Eriocheir sinensis） 肝胰腺毒性的威胁


自然环境中广泛存在的污染物 phoxim （PHO） 和纳米聚苯乙烯 （NP） 引起了人们的严重担忧。本研究评估了在环境中发现的浓度下，NP 和/或 PHO 对 Eriocheir sinensis 肝胰腺的毒性影响。在 21 天的暴露期内，亚慢性暴露于 NP 和/或 PHO 会触发肝胰腺组织学损伤。NP 、 PHO 和共暴露 （NPO） 组表现出较少的水泡状 （B） 细胞，以及空泡的出现。此外，这些暴露诱导了肝小管粘液屏障和机械屏障的损害，氧化应激相关基因、粘蛋白相关基因和 TJ 相关基因的表达改变证明了这一点。此外，观察到免疫相关基因和炎性细胞因子基因表达的改变。研究结果表明，肝胰腺炎症是由个体和联合暴露于 NP 和 PHO 引起的，并且混合暴露加剧了炎症反应。通过转录组学分析进一步研究了肝胰腺毒性的可能途径。肝胰腺炎症是由亚慢性暴露于 PHO 和共同暴露引起的;这种炎症因共暴露而加剧，并通过靶向相关基因激活 NF-κB 信号通路。总之，这项研究代表了初步记录，就我们对暴露于环境中发现的 NP 和/或 PHO 水平的有害影响的理解而言，这些有害影响会破坏甲壳类动物的肝胰腺粘液和机械屏障，引发炎症反应。这些发现突出了 NP 和/或 PHO 污染对肝胰腺健康的重要性。