OBJECTIVE: 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. METHODS: 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). RESULTS: 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. CONCLUSION: Air-borne PM2.5 could have acute toxic effects on mouse pulmonary cells and membrane tissues via immunotoxicity and oxidative stress injury.
OBJECTIVE: In order to study the acute toxicity of PM2.5 and to explore the role of immunoreaction and oxidative stress in mousepulmonary acute injury induced by PM2.5. METHODS: 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). RESULTS: 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. CONCLUSION: Air-borne PM2.5 could have acute toxic effects on mouse pulmonary cells and membrane tissues via immunotoxicity and oxidative stress injury.