Author
Listed:
- 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)
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 .
Suggested Citation
Yiling Pei & Rongfang Jiang & Yunzeng Zou & Yu Wang & Suhui Zhang & Guanghe Wang & Jinzhuo Zhao & Weimin Song, 2016.
"Effects of Fine Particulate Matter (PM 2.5 ) on Systemic Oxidative Stress and Cardiac Function in ApoE −/− Mice,"
IJERPH, MDPI, vol. 13(5), pages 1-15, May.
Handle:
RePEc:gam:jijerp:v:13:y:2016:i:5:p:484-:d:69887
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Cited by:
- Ching-Chang Cho & Wen-Yeh Hsieh & Chin-Hung Tsai & Cheng-Yi Chen & Hui-Fang Chang & Chih-Sheng Lin, 2018.
"In Vitro and In Vivo Experimental Studies of PM 2.5 on Disease Progression,"
IJERPH, MDPI, vol. 15(7), pages 1-26, July.
- Wei Liu & Minjia Zhang & Jinqiu Feng & Aiqin Fan & Yalin Zhou & Yajun Xu, 2017.
"The Influence of Quercetin on Maternal Immunity, Oxidative Stress, and Inflammation in Mice with Exposure of Fine Particulate Matter during Gestation,"
IJERPH, MDPI, vol. 14(6), pages 1-16, June.
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