期刊
ENVIRONMENTAL TOXICOLOGY
卷 31, 期 12, 页码 1996-2005出版社
WILEY
DOI: 10.1002/tox.22200
关键词
air pollutant co-exposure; heart; inflammation; endothelial dysfunction
资金
- National Science Foundation of PR China [21477070, 21377076, 21222701]
- Specialized Research Fund for the Doctoral Program of Higher Education [SRFDP, 20121401110003, 20131401110005]
SO2, NO2, and PM2.5 are typical air pollutants produced during the combustion of coal. Increasing evidence indicates that air pollution has contributed to the development and progression of heart-related diseases over the past decades. However, little experimental data and few studies of SO2, NO2, and PM2.5 co-exposure in animals exist; therefore, the relevant mechanisms underlying this phenomenon are unclear. An important characteristic of air pollution is that co-exposure persists at a low concentration throughout a lifetime. In the present study, we treated adult mice with SO2, NO2, and PM2.5 at various concentrations (0.5 mg/m(3) SO2, 0.2 mg/m(3) NO2 6 h/d, with intranasal instillation of 1 mg/kg PM2.5 every other day during these exposures; or 3.5 mg/m(3) SO2, 2 mg/m(3) NO2 6 h/d, and 10 mg/kg PM2.5 for 28 d). Blood pressure (BP), heart rate (HR), histopathological damage, and inflammatory and endothelial cytokines in the heart were assessed. The results indicate that co-exposure caused endothelial dysfunction by elevating endothelin-1 (ET-1) expression and repressing the endothelial nitric oxide synthase (eNOS) level as well as stimulating the inflammatory response by increasing the levels of cyclooxygenase2 (COX-2), inducible nitric oxide synthase (iNOS), tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). Additionally, these alterations were confirmed by histological staining. Furthermore, we observed decreased BP and increased HR after co-exposure. Our results indicate that co-exposure to SO2, NO2, and PM2.5 may be a major risk factor for cardiac disease and may induce injury to the hearts of mammals and contribute to heart disease. (C) 2015 Wiley Periodicals, Inc.
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