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

DC FieldValueLanguage
dc.contributor.author박희남-
dc.contributor.author신동천-
dc.contributor.author이문형-
dc.contributor.author정보영-
dc.contributor.author최은미-
dc.contributor.author황기철-
dc.contributor.author김창수-
dc.contributor.author박혜림-
dc.date.accessioned2014-12-19T17:43:44Z-
dc.date.available2014-12-19T17:43:44Z-
dc.date.issued2012-
dc.identifier.issn0041-008X-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/91944-
dc.description.abstractAmbient 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.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfToxicology and Applied Pharmacology-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleParticulate air pollution induces arrhythmia via oxidative stress and calcium calmodulin kinase II activation-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Life Science (의생명과학부)-
dc.contributor.googleauthorJin-Bae Kim-
dc.contributor.googleauthorChangsoo Kim-
dc.contributor.googleauthorEunmi Choi-
dc.contributor.googleauthorSanghoon Park-
dc.contributor.googleauthorHyelim Park-
dc.contributor.googleauthorHui-Nam Pak-
dc.contributor.googleauthorMoon-Hyoung Lee-
dc.contributor.googleauthorDong Chun Shin-
dc.contributor.googleauthorKi-Chul Hwang-
dc.contributor.googleauthorBoyoung Joung-
dc.identifier.doi10.1016/j.taap.2011.12.007-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01776-
dc.contributor.localIdA02096-
dc.contributor.localIdA02766-
dc.contributor.localIdA03609-
dc.contributor.localIdA04456-
dc.contributor.localIdA01042-
dc.contributor.localIdA01760-
dc.contributor.localIdA04151-
dc.relation.journalcodeJ02742-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0041008X11004649-
dc.contributor.alternativeNamePak, Hui Nam-
dc.contributor.alternativeNameShin, Dong Chun-
dc.contributor.alternativeNameLee, Moon Hyoung-
dc.contributor.alternativeNameJoung, Bo Young-
dc.contributor.alternativeNameChoi, Eun Mi-
dc.contributor.alternativeNameHwang, Ki Chul-
dc.contributor.alternativeNameKim, Chang Soo-
dc.contributor.alternativeNamePark, Hye Lim-
dc.contributor.affiliatedAuthorPak, Hui Nam-
dc.contributor.affiliatedAuthorShin, Dong Chun-
dc.contributor.affiliatedAuthorLee, Moon Hyoung-
dc.contributor.affiliatedAuthorJoung, Bo Young-
dc.contributor.affiliatedAuthorHwang, Ki Chul-
dc.contributor.affiliatedAuthorKim, Chang Soo-
dc.contributor.affiliatedAuthorPark, Hye Lim-
dc.contributor.affiliatedAuthorChoi, Eun Mi-
dc.citation.volume259-
dc.citation.number1-
dc.citation.startPage66-
dc.citation.endPage73-
dc.identifier.bibliographicCitationToxicology and Applied Pharmacology, Vol.259(1) : 66-73, 2012-
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

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