Effects of Fine Particulate Matter PM2.5 on Systemic Oxidative Stress and Cardiac Function in ApoE−-− MiceReport as inadecuate




Effects of Fine Particulate Matter PM2.5 on Systemic Oxidative Stress and Cardiac Function in ApoE−-− Mice - Download this document for free, or read online. Document in PDF available to download.

1

Department of Environmental Health, School of Public Health and Key Laboratory of Public Health Safety, Fudan University, Shanghai 200032, China

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Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, China

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Pharmacology and Toxicology Department, Shanghai Institute for Food and Drug Control, Shanghai 201203, China

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Department of Hygienic Toxicology, College of Public Health, Harbin Medical University, Harbin 150081, China





*

Authors to whom correspondence should be addressed.



Academic Editor: Paul B. Tchounwou

Abstract Aim: In this study, we aimed to explore the toxic mechanisms of cardiovascular injuries induced by ambient fine particulate matter PM2.5 in atherosclerotic-susceptible ApoE−-− mice. An acute toxicological animal experiment was designed with PM2.5 exposure once a day, every other day, for three days. Methods: ApoE−-− and C57BL-6 mice were randomly categorized into four groups, respectively n = 6: one control group, three groups exposed to PM2.5 alone at low-, mid-, and high-dose 3, 10, or 30 mg-kg b.w

Heart rate HR and electrocardiogram ECG were monitored before instillation of PM2.5 and 24 h after the last instillation, respectively. Cardiac function was monitored by echocardiography Echo after the last instillation. Biomarkers of systemic oxidative injuries MDA, SOD, heart oxidative stress MDA, SOD, and NADPH oxidase subunits p22phox, p47phox mRNA and protein expression were analyzed in mice. The results showed that PM2.5 exposure could trigger the significant increase of MDA, and induce the decrease of heart rate variability HRV, a marker of cardiac autonomic nervous system ANS function with a dose–response manner. Meanwhile, abnormal ECG types were monitored in mice after exposure to PM2.5. The expression of cytokines related with oxidative injuries, and mRNA and protein expression of NADPH, increased significantly in ApoE−-− mice in the high-dose group when compared with the dose-matched C57BL6 mice, but no significant difference was observed at Echo. In conclusion, PM2.5 exposure could cause oxidative and ANS injuries, and ApoE−-− mice displayed more severe oxidative effects induced by PM2.5. View Full-Text

Keywords: PM2.5; atherosclerosis; autonomic nervous system ANS; echocardiography Echo; oxidative stress PM2.5; atherosclerosis; autonomic nervous system ANS; echocardiography Echo; oxidative stress





Author: Yiling Pei 1, Rongfang Jiang 1, Yunzeng Zou 2, Yu Wang 3, Suhui Zhang 3, Guanghe Wang 4, Jinzhuo Zhao 1,* and Weimin Song 1,*

Source: http://mdpi.com/



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