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上皮细胞和巨噬细胞溶解导致的铟离子释放导致氧化铟纳米颗粒引起的肺毒性。

The Release of Indium Ion Derived from Epithelial Cells and Macrophages Solubilization Contribute to Pneumotoxicity Induced by Indium Oxide Nanoparticles.

机构信息

Key Laboratory of Environmental Medicine Engineering of Ministry of Education, School of Public Health, Southeast University, Nanjing, Jiangsu 210000, China.

Centers for Disease Control and Prevention, Nanjing, Jiangsu 210093, China.

出版信息

J Nanosci Nanotechnol. 2021 Dec 1;21(12):6007-6015. doi: 10.1166/jnn.2021.19498.

DOI:10.1166/jnn.2021.19498
PMID:34229798
Abstract

Occupational exposure to indium oxide and indium containing particles has been associated with the development of severe lung diseases called "indium lung." According to the survey of occupational hygiene, indium oxide nanoparticles have been identified in the workplaces and the lungs of workers. To date, the potential mechanism of the pneumotoxicity has been poorly understood and no effective therapies are available against "indium lung." Our present study reported that the exposure of indium oxide nanoparticles damaged lung epithelial cells and alveolar macrophages and induced pulmonary alveolar proteinosis and inflammation in rats. In the 8-week post-exposure period, the indium oxide nanoparticles still mostly accumulated in the lungs and then persistently release indium ions in two months after exposure. , the epithelial cells show the greater potential for release of indium ions from indium oxide nanoparticles compared with the macrophages. EDTA-2Na, a metal chelating agent expected to remove the indium ions, was found to significantly reduced the cytotoxicity of indium oxide nanoparticles. Herein, the pneumotoxicity may be attributed to the slow and incremental release of indium ions from indium oxide nanoparticles primary dissolved by epithelial cells and macrophages, at least partially. The study may provide some insights to the pathogenicity mechanisms of "indium lung" and some clues against the health hazards of occupational inhaled indium oxide nanoparticles at the workplaces.

摘要

职业性接触氧化铟和含铟颗粒与严重肺部疾病(称为“铟肺”)的发生有关。根据职业卫生调查,工作场所和工人的肺部已发现氧化铟纳米颗粒。迄今为止,对其引起的肺毒性的潜在机制仍知之甚少,也没有有效的治疗方法。我们目前的研究表明,氧化铟纳米颗粒的暴露会损害肺上皮细胞和肺泡巨噬细胞,并在大鼠中诱导肺泡蛋白沉积症和炎症。在暴露后的 8 周期间,氧化铟纳米颗粒仍主要积聚在肺部,并在暴露后两个月内持续释放铟离子。相比之下,上皮细胞比巨噬细胞更有潜力从氧化铟纳米颗粒中释放铟离子。乙二胺四乙酸二钠(EDTA-2Na)是一种预期能去除铟离子的金属螯合剂,被发现可显著降低氧化铟纳米颗粒的细胞毒性。因此,这种肺毒性可能归因于上皮细胞和巨噬细胞最初溶解的氧化铟纳米颗粒中缓慢且逐渐释放的铟离子,至少部分原因是这样。该研究可能为“铟肺”的发病机制提供一些见解,并为应对工作场所职业性吸入氧化铟纳米颗粒对健康的危害提供一些线索。

相似文献

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The Release of Indium Ion Derived from Epithelial Cells and Macrophages Solubilization Contribute to Pneumotoxicity Induced by Indium Oxide Nanoparticles.上皮细胞和巨噬细胞溶解导致的铟离子释放导致氧化铟纳米颗粒引起的肺毒性。
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引用本文的文献

1
A case report of Indium lung with progressive emphysema and fibrosis underwent lung unilateral transplantation 20 years after the end of the exposure.铟肺伴进行性肺气肿和肺纤维化 1 例,接触结束 20 年后行单侧肺移植。
Diagn Pathol. 2023 Jan 28;18(1):10. doi: 10.1186/s13000-023-01303-1.