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Particulate air pollution induces arrhythmia via oxidative stress and calcium calmodulin kinase II activation

Authors
 Jin-Bae Kim  ;  Changsoo Kim  ;  Eunmi Choi  ;  Sanghoon Park  ;  Hyelim Park  ;  Hui-Nam Pak  ;  Moon-Hyoung Lee  ;  Dong Chun Shin  ;  Ki-Chul Hwang  ;  Boyoung Joung 
Citation
 Toxicology and Applied Pharmacology, Vol.259(1) : 66-73, 2012 
Journal Title
 Toxicology and Applied Pharmacology 
ISSN
 0041-008X 
Issue Date
2012
Abstract
Ambient particulate matter (PM) can increase the incidence of arrhythmia. However, the arrhythmogenic mechanism of PM is poorly understood. This study investigated the arrhythmogenic mechanism of PM. In Sprague-Dawley rats, QT interval was increased from 115.0±14.0 to 142.1±18.4ms (p=0.02) after endotracheal exposure of DEP (200μg/ml for 30min, n=5). Ventricular premature contractions were more frequently observed after DEP exposure (100%) than baseline (20%, p=0.04). These effects were prevented by pretreatment of N-acetylcysteine (NAC, 5mmol/L, n=3). In 12 Langendorff-perfused rat hearts, DEP infusion of 12.5μg/ml for 20min prolonged action potential duration (APD) at only left ventricular base increasing apicobasal repolarization gradients. Spontaneous early afterdepolarization (EAD) and ventricular tachycardia (VT) were observed in 8 (67%) and 6 (50%) hearts, respectively, versus no spontaneous triggered activity or VT in any hearts before DEP infusion. DEP-induced APD prolongation, EAD and VT were successfully prevented with NAC (5mmol/L, n=5), nifedipine (10μmol/L, n=5), and active Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) blockade, KN 93 (1μmol/L, n=5), but not by thapsigargin (200nmol/L) plus ryanodine (10μmol/L, n=5) and inactive CaMKII blockade, KN 92 (1μmol/L, n=5). In neonatal rat cardiomyocytes, DEP provoked ROS generation in dose dependant manner. DEP (12.5μg/ml) induced apoptosis, and this effect was prevented by NAC and KN 93. Thus, this study shows that in vivo and vitro exposure of PM induced APD prolongation, EAD and ventricular arrhythmia. These effects might be caused by oxidative stress and CaMKII activation.
Full Text
http://www.sciencedirect.com/science/article/pii/S0041008X11004649
DOI
10.1016/j.taap.2011.12.007
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Preventive Medicine and Public Health (예방의학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
Yonsei Authors
Kim, Chang Soo(김창수) ORCID logo https://orcid.org/0000-0002-5940-5649
Park, Hye Lim(박혜림)
Pak, Hui Nam(박희남) ORCID logo https://orcid.org/0000-0002-3256-3620
Shin, Dong Chun(신동천) ORCID logo https://orcid.org/0000-0003-4252-2280
Lee, Moon Hyoung(이문형) ORCID logo https://orcid.org/0000-0002-7268-0741
Joung, Bo Young(정보영) ORCID logo https://orcid.org/0000-0001-9036-7225
Choi, Eun Mi(최은미)
Hwang, Ki Chul(황기철)
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URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/91944
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