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接触胶体二氧化硅引起的急性肺毒性:小鼠中粒径依赖性病理变化

Acute pulmonary toxicity caused by exposure to colloidal silica: particle size dependent pathological changes in mice.

作者信息

Kaewamatawong Theerayuth, Kawamura Natsuko, Okajima Mina, Sawada Masumi, Morita Takehito, Shimada Akinori

机构信息

Department of Veterinary Pathology, Tottori University Minami 4-101, Koyama, Tottori-shi, Tottori 680-0945, Japan.

出版信息

Toxicol Pathol. 2005;33(7):743-9. doi: 10.1080/01926230500416302.

Abstract

To compare the pulmonary toxicity between ultrafine colloidal silica particles (UFCSs) and fine colloidal silica particles (FCSs), mice were intratracheally instilled with 3 mg of 14 nm UFCSs and 230 nm FCSs and pathologically examined from 30 minutes to 24 hour postexposure. Histopathologically, lungs exposed to both sizes of particles showed bronchiolar degeneration and necrosis, neutrophilic inflammation in alveoli with alveolar type II cell swelling and particle-laden alveolar macrophage accumulation. UFCSs, however, induced extensive alveolar hemorrhage compared to FCSs from 30 minutes onwards. UFCSs also caused more severe bronchiolar epithelial cell necrosis and neutrophil influx in alveoli than FCSs at 12 and 24 hours postexposure. Laminin positive immunolabellings in basement membranes of bronchioles and alveoli of UFCSs treated animals was weaker than those of FCSs-treated animals in all observation times. Electron microscopy demonstrated UFCSs and FCSs on bronchiolar and alveolar wall surface as well as in the cytoplasm of alveolar epithelial cells, alveolar macrophages and neutrophils. Type I alveolar epithelial cell erosion with basement membrane damage in UFCSs treated animals was more severe than those in FCSs-treated animals. At 12 and 24 hours postexposure, bronchiolar epithelial cells in UFCSs-treated animals showed more intense vacuolation and necrosis compared to FCSs-treated animals. These findings suggest that UFCSs have greater ability to induce lung inflammation and tissue damages than FCSs.

摘要

为比较超细胶体二氧化硅颗粒(UFCSs)和细胶体二氧化硅颗粒(FCSs)之间的肺毒性,给小鼠气管内滴注3毫克14纳米的UFCSs和230纳米的FCSs,并在暴露后30分钟至24小时进行病理检查。组织病理学上,暴露于这两种颗粒大小的肺均显示细支气管变性和坏死,肺泡内中性粒细胞炎症伴II型肺泡细胞肿胀以及含颗粒的肺泡巨噬细胞积聚。然而,从30分钟起,与FCSs相比,UFCSs引起广泛的肺泡出血。在暴露后12小时和24小时,UFCSs还比FCSs导致更严重的细支气管上皮细胞坏死和肺泡内中性粒细胞流入。在所有观察时间内,UFCSs处理动物的细支气管和肺泡基底膜中层粘连蛋白阳性免疫标记比FCSs处理动物的弱。电子显微镜显示UFCSs和FCSs位于细支气管和肺泡壁表面以及肺泡上皮细胞、肺泡巨噬细胞和中性粒细胞的细胞质中。UFCSs处理动物的I型肺泡上皮细胞侵蚀伴基底膜损伤比FCSs处理动物的更严重。在暴露后12小时和24小时,与FCSs处理动物相比,UFCSs处理动物的细支气管上皮细胞显示出更强烈的空泡化和坏死。这些发现表明,UFCSs比FCSs具有更强的诱导肺部炎症和组织损伤的能力。

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