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镍纳米粒子对鳗鱼肝细胞 HEPA-E1 毒性的细胞和分子机制:新喀里多尼亚采矿活动中镍释放影响的说明。

Cellular and molecular mechanisms of NiONPs toxicity on eel hepatocytes HEPA-E1: An illustration of the impact of Ni release from mining activity in New Caledonia.

机构信息

Univ. Bordeaux, 146, rue Léo Saignat, Bordeaux, F-33076, France; Inserm U 1045, Centre de Recherche Cardio-Thoracique, avenue du Haut Lêveque, Pessac, F-33604, France; Univ. Bordeaux, CNRS, EPHE, UMR EPOC 5805, F-33615, Pessac, France.

Univ. Bordeaux, 146, rue Léo Saignat, Bordeaux, F-33076, France; Inserm U 1045, Centre de Recherche Cardio-Thoracique, avenue du Haut Lêveque, Pessac, F-33604, France; CHU de Bordeaux, Service d'exploration fonctionnelle respiratoire, Service de Pédiatrie médicale, Bordeaux, F-33076, France.

出版信息

Chemosphere. 2022 Sep;303(Pt 2):135158. doi: 10.1016/j.chemosphere.2022.135158. Epub 2022 May 28.

DOI:10.1016/j.chemosphere.2022.135158
PMID:35640691
Abstract

Anthropic activities such as open pit mining, amplify the natural erosion of metals contained in the soils, particularly in New Caledonia, leading to atmospheric emission of nickel oxide nanoparticles (NiONPs). These particles are produced during extraction end up in aquatic ecosystems through deposition or leaching in the rivers. Despite alarming freshwater Ni concentrations, only few studies have focused on the cellular and molecular mechanisms of NiONPs toxicity on aquatic organisms and particularly on eels. Those fish are known to be sensitive to metal contamination, especially their liver, which is a key organ for lipid metabolism, detoxification and reproduction. The objective of this study was to assess in vitro the cytotoxic effects of NiONPs on Anguilla japonica hepatocytes, HEPA-E1. HEPA-E1 were exposed to NiONPs (0.5-5 μg/cm) for 4 or 24 h. Several endpoints were studied: (i) viability, (ii) ROS production, SOD activity and selected anti-oxidant genes expression, (iii) inflammation, (iv) calcium signalling, (v) mitochondrial function and (vi) apoptosis. The results evidenced that NiONPs induce a decrease of cell viability and an increase in oxidative stress with a significant superoxide anion production. An increase of mitochondrial calcium concentration and a decrease of mitochondrial membrane potential were observed, leading to apoptosis. These results underline the potential toxic impact of NiONPs on eels living in mining areas. Therefore, eel exposure to NiONPs can affect their migration and reproduction in New Caledonia.

摘要

人为活动,如露天采矿,会加剧土壤中金属的自然侵蚀,特别是在新喀里多尼亚,导致氧化镍纳米颗粒(NiONPs)释放到大气中。这些颗粒是在提取过程中产生的,最终通过沉积或河流浸出进入水生生态系统。尽管淡水镍浓度令人震惊,但只有少数研究关注 NiONPs 对水生生物,特别是鳗鱼的细胞和分子毒性机制。这些鱼类已知对金属污染敏感,特别是它们的肝脏,肝脏是脂质代谢、解毒和繁殖的关键器官。本研究的目的是评估 NiONPs 对日本鳗鲡肝细胞(HEPA-E1)的体外细胞毒性。HEPA-E1 暴露于 NiONPs(0.5-5μg/cm)4 或 24 小时。研究了几个终点:(i)细胞活力,(ii)ROS 产生、SOD 活性和选定抗氧化基因表达,(iii)炎症,(iv)钙信号,(v)线粒体功能和(vi)细胞凋亡。结果表明,NiONPs 降低细胞活力并增加氧化应激,导致超氧阴离子产生显著增加。观察到线粒体钙离子浓度增加和线粒体膜电位降低,导致细胞凋亡。这些结果强调了 NiONPs 对生活在矿区的鳗鱼的潜在毒性影响。因此,鳗鱼暴露于 NiONPs 可能会影响它们在新喀里多尼亚的迁徙和繁殖。

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