Hubei Key Laboratory of Multi-media Pollution Cooperative Control in Yangtze Basin, School of Environmental Science & Engineering, Huazhong University of Science and Technology (HUST), Wuhan, Hubei Province 430074, China.
State Key Laboratory of Freshwater Ecology and Biotechnology and Key Laboratory of Aquaculture Disease Control, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, Hubei Province 430072, China.
Sci Total Environ. 2024 Oct 20;948:174737. doi: 10.1016/j.scitotenv.2024.174737. Epub 2024 Jul 14.
In recent years, there has been a growing focus on the toxicity and mortality induced by nanoplastics (NPs) in aquatic organisms. However, studies investigating mechanisms underlying oxidative stress (OS), apoptosis, and inflammation induced by NPs in fish remain limited. This study observed that polystyrene NPs (PS-NPs) were accumulated into zebrafish larvae and zebrafish embryonic fibroblast (ZF4 cells), accompanied by the occurrence of pathological damage both at the cellular and tissue-organ level. Additionally, the transcriptional up-regulation of NADPH oxidases (NOXs) and subsequent excessive generation of reactive oxygen species (ROS) resulted in notable changes in the relative mRNA and protein expression levels associated with antioxidant oxidase systems in larvae. Furthermore, the study identified the impact of NPs on mitochondrial ultrastructural, resulting in mitochondrial depolarization and downregulation of mRNA expression related to the electron transport chain due to excessive ROS generation. Short-term exposure to NPs also triggered apoptosis and inflammation in zebrafish larvae, evident from significant up-regulation in mRNA expressions of proapoptotic factors and NF-κB proinflammatory signaling pathway, as well as increased transcription and protein levels of pro-inflammatory factors in larvae. Inhibition of intracellular excessive ROS effectively reduced the induction of apoptosis, NF-κB P65 nuclear migration levels, and cytokine secretion, underscoring OS as a pivotal factor throughout the process of apoptosis and inflammatory responses induced by NPs. This research significantly advances our comprehension of biological effects and underlying mechanisms of NPs in freshwater fish.
近年来，人们越来越关注纳米塑料（NPs）在水生生物中引起的毒性和死亡率。然而，研究纳米颗粒诱导鱼类氧化应激（OS）、细胞凋亡和炎症的机制的研究仍然有限。本研究观察到聚苯乙烯纳米颗粒（PS-NPs）在斑马鱼幼虫和斑马鱼胚胎成纤维细胞（ZF4 细胞）中积累，并在细胞和组织器官水平上发生病理损伤。此外，NADPH 氧化酶（NOXs）的转录上调和随后活性氧（ROS）的过度产生导致幼虫抗氧化氧化酶系统相关的相对 mRNA 和蛋白表达水平发生显著变化。此外，该研究还发现 NPs 对线粒体超微结构的影响，导致线粒体去极化和与电子传递链相关的 mRNA 表达下调，这是由于 ROS 过度产生。 NPs 的短期暴露也在斑马鱼幼虫中引发了细胞凋亡和炎症，这表现在促凋亡因子和 NF-κB 促炎信号通路的 mRNA 表达水平显著上调，以及幼虫中促炎因子的转录和蛋白水平增加。抑制细胞内过量的 ROS 可有效减少细胞凋亡、NF-κB P65 核迁移水平和细胞因子分泌的诱导，这表明 OS 是 NPs 诱导细胞凋亡和炎症反应过程中的关键因素。这项研究极大地提高了我们对淡水鱼类中 NPs 的生物学效应和潜在机制的理解。
