Jiang Zhihai, Song Weimin, Zhou Xiaoyu, Zhang Yifan
Department of Environment Health, School of Public Health, Fudan University, Shanghai 200032, China.
Wei Sheng Yan Jiu. 2004 May;33(3):264-6.
In order to study the acute toxicity of PM2.5 and to explore the role of immunoreaction and oxidative stress in mouse pulmonary acute injury induced by PM2.5.
Kunming mice were randomly divided into five groups including blank control group, saline control group, three level PM2.5 (low, middle and high) groups. Three level PM2.5 groups were inoculated with suspensions of PM2.5 via trachea for 24 hours and saline control group were inoculated saline, Pulmonary pathological injury and bronchoalveolar lavage fluid (BALF) of all mice were later examined, including the level of LDH, AKP, ACP, ALB, NO, NOS, MDA, SOD, activities of TNF-alpha, IL-1 and phagocytosis of Alveolar macrophages (AM).
The amount of LDH, AKP, ACP, ALB, NO, NOS, MDA and activities of TNF-alpha, IL-1 in exposed groups were significantly higher than those in control(P < 0.05), and at the same time the amount of SOD and phagocytosis of AM decreased significantly (P < 0.05). Dose-response relationships were observed in all indexes.
Air-borne PM2.5 could have acute toxic effects on mouse pulmonary cells and membrane tissues via immunotoxicity and oxidative stress injury.
研究细颗粒物（PM2.5）的急性毒性，探讨免疫反应和氧化应激在PM2.5致小鼠肺急性损伤中的作用。
将昆明小鼠随机分为五组，包括空白对照组、生理盐水对照组、三个剂量水平的PM2.5（低、中、高）组。三个剂量水平的PM2.5组经气管接种PM2.5悬液24小时，生理盐水对照组接种生理盐水，随后检测所有小鼠的肺病理损伤及支气管肺泡灌洗液（BALF），包括乳酸脱氢酶（LDH）、碱性磷酸酶（AKP）、酸性磷酸酶（ACP）、白蛋白（ALB）、一氧化氮（NO）、一氧化氮合酶（NOS）、丙二醛（MDA）、超氧化物歧化酶（SOD）水平，肿瘤坏死因子-α（TNF-α）、白细胞介素-1（IL-1）活性及肺泡巨噬细胞（AM）吞噬功能。
各暴露组的LDH、AKP、ACP、ALB、NO、NOS、MDA含量及TNF-α、IL-1活性均显著高于对照组（P<0.05），同时SOD含量及AM吞噬功能显著降低（P<0.05）。所有指标均呈现剂量-反应关系。
空气中的PM2.5可通过免疫毒性和氧化应激损伤对小鼠肺细胞和膜组织产生急性毒性作用。
