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聚苯乙烯纳米微塑料加重斑马鱼胚胎中氨诱导的神经毒性作用。

Polystyrene Nanomicroplastics Aggravate Ammonia-Induced Neurotoxic Effects in Zebrafish Embryos.

作者信息

Xing Dan, Zheng Wenting, Zhou Huiming, Li Guangyu, Li Yan, Jia Jingwen, Liu Haoling, Luan Ning, Liu Xiaolin

机构信息

College of Fisheries, Huazhong Agricultural University, Wuhan 430070, China.

CHN Energy Dadu River Hydropower Development Co., Ltd., Chengdu 610000, China.

出版信息

Toxics. 2024 Nov 26;12(12):853. doi: 10.3390/toxics12120853.

DOI:10.3390/toxics12120853
PMID:39771068
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11679152/
Abstract

The highly hazardous chemical ammonia has been proven to be absorbed by nanoparticles, thereby exerting highly toxic effects on aquatic organisms. As a ubiquitous pollutant in aquatic environments, polystyrene nanomicroplastics (PSNPs) have shown strong adsorption capacity due to their large surface area. Therefore, the potential joint effects of ammonia and PSNPs need to be clarified. In this study, zebrafish embryos were exposed to a water solution with ammonia concentrations (0, 0.1, 1, and 10 mg/L) with or without PSNP (100 μg/L) treatment up to 120 hpf. The results showed that combined exposure increased the accumulation of ammonia and obviously reduced the locomotor speed of zebrafish larvae compared with exposure to ammonia alone. Further studies indicated that PSNPs can aggravate ammonia-induced neurotoxicity by altering the cholinergic system, dopaminergic neurons, and the retinal structure in zebrafish larvae. In addition, our results revealed that ammonia caused significant alterations in the expression of genes related to neurodevelopment and retinal development, and PSNPs exacerbated this adverse effect. In conclusion, PSNPs can aggravate ammonia-induced neurotoxicity in the early stage of zebrafish and their associated health risk to aquatic animals should not be underestimated. The main contribution of this article lies in revealing the synergistic neurotoxicity of ammonia and PSNPs in the early stage of zebrafish. Moreover; it emphasizes that the associated health risks to aquatic animals should not be underestimated.

摘要

剧毒化学物质氨已被证明可被纳米颗粒吸收,从而对水生生物产生高毒性作用。作为水环境中普遍存在的污染物,聚苯乙烯纳米微塑料(PSNPs)因其巨大的表面积而表现出很强的吸附能力。因此,需要阐明氨和PSNPs的潜在联合效应。在本研究中,将斑马鱼胚胎暴露于含有氨浓度(0、0.1、1和10 mg/L)的水溶液中,分别进行有无PSNP(100 μg/L)处理,直至120 hpf。结果表明,与单独暴露于氨相比,联合暴露增加了氨的积累,并明显降低了斑马鱼幼体的运动速度。进一步研究表明,PSNPs可通过改变斑马鱼幼体的胆碱能系统、多巴胺能神经元和视网膜结构来加重氨诱导的神经毒性。此外,我们的结果显示,氨导致与神经发育和视网膜发育相关的基因表达发生显著变化,而PSNPs加剧了这种不良影响。总之,PSNPs可在斑马鱼早期加重氨诱导的神经毒性,其对水生动物的相关健康风险不容小觑。本文的主要贡献在于揭示了氨和PSNPs在斑马鱼早期的协同神经毒性。此外,强调了对水生动物的相关健康风险不容小觑。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49df/11679152/73999f2d3723/toxics-12-00853-g008.jpg
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本文引用的文献

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Hormetic Nutrition and Redox Regulation in Gut-Brain Axis Disorders.肠道-脑轴疾病中的应激性营养与氧化还原调节
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Dihalogenated nitrophenols exposure induces developmental neurotoxicity in zebrafish embryo.
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Nanoplastics aggravated TDCIPP-induced transgenerational developmental neurotoxicity in zebrafish depending on the involvement of the dopamine signaling pathway.纳米塑料加剧了三氯双酚 A 对斑马鱼跨代发育神经毒性的作用,其作用机制与多巴胺信号通路有关。
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Investigation of ammonia-induced lethal toxicity toward ion regulation in zebrafish embryos.研究氨诱导斑马鱼胚胎离子调节致死毒性。
Comp Biochem Physiol C Toxicol Pharmacol. 2024 Feb;276:109807. doi: 10.1016/j.cbpc.2023.109807. Epub 2023 Nov 25.
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Unraveling the mechanisms of perfluorooctanesulfonic acid-induced dopaminergic neurotoxicity and microglial activation in developing zebrafish.揭示全氟辛烷磺酸诱导发育中斑马鱼多巴胺能神经毒性和小胶质细胞激活的机制。
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Hypoplasia of dopaminergic neurons by hypoxia-induced neurotoxicity is associated with disrupted swimming development of larval zebrafish.缺氧诱导的神经毒性导致的多巴胺能神经元发育不全与斑马鱼幼体游泳发育障碍有关。
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Sublethal ammonia induces alterations of emotions, cognition, and social behaviors in zebrafish (Danio rerio).亚致死浓度氨可诱导斑马鱼(Danio rerio)的情绪、认知和社交行为改变。
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