Effects of Fine Particulate Matter (PM 2.5 ) on Systemic Oxidative Stress and Cardiac Function in ApoE ?/? Mice

Yiling Pei, Rongfang Jiang, Yunzeng Zou, Yu Wang, Suhui Zhang, Guanghe Wang, Jinzhuo Zhao and Weimin Song
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Yiling Pei: Department of Environmental Health, School of Public Health and Key Laboratory of Public Health Safety, Fudan University, Shanghai 200032, China
Rongfang Jiang: Department of Environmental Health, School of Public Health and Key Laboratory of Public Health Safety, Fudan University, Shanghai 200032, China
Yunzeng Zou: Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, China
Yu Wang: Pharmacology and Toxicology Department, Shanghai Institute for Food and Drug Control, Shanghai 201203, China
Suhui Zhang: Pharmacology and Toxicology Department, Shanghai Institute for Food and Drug Control, Shanghai 201203, China
Guanghe Wang: Department of Hygienic Toxicology, College of Public Health, Harbin Medical University, Harbin 150081, China
Jinzhuo Zhao: Department of Environmental Health, School of Public Health and Key Laboratory of Public Health Safety, Fudan University, Shanghai 200032, China
Weimin Song: Department of Environmental Health, School of Public Health and Key Laboratory of Public Health Safety, Fudan University, Shanghai 200032, China

IJERPH, 2016, vol. 13, issue 5, 1-15

Abstract: Aim: In this study, we aimed to explore the toxic mechanisms of cardiovascular injuries induced by ambient fine particulate matter (PM 2.5 ) in atherosclerotic-susceptible ApoE ?/? mice. An acute toxicological animal experiment was designed with PM 2.5 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 PM 2.5 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 PM 2.5 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 NAD(P)H oxidase subunits (p22phox, p47phox) mRNA and protein expression were analyzed in mice. The results showed that PM 2.5 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 PM 2.5 . 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, PM 2.5 exposure could cause oxidative and ANS injuries, and ApoE ?/? mice displayed more severe oxidative effects induced by PM 2.5 .

Keywords: PM 2.5; atherosclerosis; autonomic nervous system (ANS); echocardiography (Echo); oxidative stress (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2016
References: View complete reference list from CitEc
Citations: View citations in EconPapers (2)

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