Acute and subacute pulmonary toxicity of low dose of ultrafine colloidal silica particles in mice after intratracheal instillation
Acute and subacute pulmonary toxicity of low dose of ultrafine colloidal silica particles in mice after intratracheal instillation
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DOI：
10.1080/01926230601094552
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发表时间：
2006-01-01
影响因子：
1.5
通讯作者：
Takano, Hirohisa
中科院分区：
文献类型：
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作者：
Kaewamatawong, Theerayuth;Shimada, Akinori;Takano, Hirohisa
为研究低剂量超细硅胶颗粒（UFCs）的急性和亚急性肺毒性，将0、0.3、3、10、30和100 μ g的UFCs注入小鼠气管内。于给药后第3天测定支气管肺泡灌洗液（BALF）中细胞和生化指标、组织学改变及体重。暴露于30或100 μ g的UFCS产生中度至重度的肺部炎症和组织损伤。为了研究时间反应，向小鼠滴注30 μ g UFCS，并在暴露后1至30天间隔处死。UFCSs在急性期引起中度肺部炎症和BALF指标的损伤;然而，这些变化在实验期间逐渐消退直至恢复。伴随的组织病理学和层粘连蛋白免疫组化结果通常与BALF数据相关。UFCS处理的动物中的TUNEL分析显示在所有观察时间肺实质中的凋亡指数显著增加。8-OHdG表达发生在肺上皮细胞和活化的巨噬细胞中，这与UFCS处理的小鼠的肺病变相关。这些发现表明，滴注小剂量的UFCS会引起短暂的急性中度肺部炎症和组织损伤。氧化应激和细胞凋亡可能是肺组织损伤的基础。
To study the acute and subacute lung toxicity of low dose of ultrafine colloidal silica particles (UFCSs), mice were intratracheally instilled with 0, 0.3, 3, 10, 30 or 100 mu g of UFCSs. Cellular and biochemical parameters in bronchoalveolar lavage fluid (BALF), histological alteration and the body weight were determined at 3 days after instillation. Exposure to 30 or 100 mu g of UFCSs produced moderate to severe pulmonary inflammation and tissue injury. To investigate the time response, mice were instilled with 30 mu g of UFCSs and sacrificed at intervals from 1 to 30 days post-exposure. UFCSs induced moderate pulmonary inflammation and injury on BALF indices at acute period; however, these changes gradually regressed until recovery during the experiment. Concomitant histopathological and laminin immunohistochemical findings generally correlated to BALF data. TUNEL analyses in UFCSs-treated animals showed a significant increase of the apoptotic index in lung parenchyma at all observation times. 8-OHdG expression occurred in lung epithelial cells and activated macrophages, which correlated to lung lesions in UFCSs-treated mice. These findings suggest that instillation of a small dose of UFCSs causes transient acute moderate lung inflammation and tissue damage. Oxidative stress and apoptosis may underlie the lung tissue injury induction.