3 179

Cited 0 times in

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.
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/91944
Full Text
http://www.sciencedirect.com/science/article/pii/S0041008X11004649
DOI
10.1016/j.taap.2011.12.007
Appears in Collections:
1. Journal Papers (연구논문) > 1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부)
1. Journal Papers (연구논문) > 1. College of Medicine (의과대학) > Dept. of Preventive Medicine and Public Health (예방의학교실)
1. Journal Papers (연구논문) > 1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실)
1. Journal Papers (연구논문) > 1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원)
Yonsei Authors
김창수(Kim, Chang Soo)
박혜림(Park, Hye Lim)
박희남(Pak, Hui Nam) ORCID logo https://orcid.org/0000-0002-3256-3620
신동천(Shin, Dong Chun)
이문형(Lee, Moon Hyoung) ORCID logo https://orcid.org/0000-0002-7268-0741
정보영(Joung, Bo Young)
최은미(Choi, Eun Mi)
황기철(Hwang, Ki Chul)
Export
RIS (EndNote)
XLS (Excel)
XML
사서에게 알리기
  feedback

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse