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

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 end...

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Published in:Toxicology and applied pharmacology 2012-02, Vol.259 (1), p.66-73
Main Authors: Kim, Jin-Bae, Kim, Changsoo, Choi, Eunmi, Park, Sanghoon, Park, Hyelim, Pak, Hui-Nam, Lee, Moon-Hyoung, Shin, Dong Chun, Hwang, Ki-Chul, Joung, Boyoung
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cited_by cdi_FETCH-LOGICAL-c413t-e88281428b882042ebf54128e8fd670c61510ee012e2c249e6ac5b8a2afa35b73
cites cdi_FETCH-LOGICAL-c413t-e88281428b882042ebf54128e8fd670c61510ee012e2c249e6ac5b8a2afa35b73
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container_title Toxicology and applied pharmacology
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creator Kim, Jin-Bae
Kim, Changsoo
Choi, Eunmi
Park, Sanghoon
Park, Hyelim
Pak, Hui-Nam
Lee, Moon-Hyoung
Shin, Dong Chun
Hwang, Ki-Chul
Joung, Boyoung
description 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 Ca2+/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. ► The ambient PM consistently prolonged repolarization. ► The ambient PM induced triggered activity and ventricular arrhythmia. ► These effects were prevented by antioxidants, ICaL blockade and CaMKII blockade. ► The ambient PM can induce arrhythmia via oxidative stress and activation of CaMKII.
doi_str_mv 10.1016/j.taap.2011.12.007
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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 Ca2+/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. ► The ambient PM consistently prolonged repolarization. ► The ambient PM induced triggered activity and ventricular arrhythmia. ► These effects were prevented by antioxidants, ICaL blockade and CaMKII blockade. ► The ambient PM can induce arrhythmia via oxidative stress and activation of CaMKII.</description><identifier>ISSN: 0041-008X</identifier><identifier>EISSN: 1096-0333</identifier><identifier>DOI: 10.1016/j.taap.2011.12.007</identifier><identifier>PMID: 22197715</identifier><identifier>CODEN: TXAPA9</identifier><language>eng</language><publisher>Amsterdam: Elsevier Inc</publisher><subject>60 APPLIED LIFE SCIENCES ; Acetylcysteine - pharmacology ; Action Potentials - drug effects ; Air ; Air Pollutants - toxicity ; AIR POLLUTION ; Animals ; Animals, Newborn ; ANTIOXIDANTS ; APOPTOSIS ; Apoptosis - drug effects ; Arrhythmias, Cardiac - chemically induced ; Arrhythmias, Cardiac - enzymology ; Arrhythmias, Cardiac - metabolism ; Arrhythmias, Cardiac - prevention &amp; control ; Biological and medical sciences ; BIOLOGICAL STRESS ; Ca2 +/calmodulin-dependent protein kinase II ; CALCIUM ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism ; CALMODULIN ; Cardiac dysrhythmias ; Cardiology. Vascular system ; Cells, Cultured ; Dose-Response Relationship, Drug ; Environmental pollutants toxicology ; Enzyme Activation ; HEART ; Immunoblotting ; Immunohistochemistry ; IN VIVO ; INFUSION ; Male ; Medical sciences ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism ; OXIDATION ; Oxidative stress ; Oxidative Stress - drug effects ; OXYGEN ; Particulate matter ; Particulate Matter - toxicity ; RATS ; Rats, Sprague-Dawley ; Reactive Oxygen Species - metabolism ; Toxicology ; Vehicle Emissions - toxicity ; Ventricular fibrillation ; Ventricular Premature Complexes - chemically induced ; Ventricular Premature Complexes - enzymology ; Ventricular Premature Complexes - metabolism ; Ventricular Premature Complexes - prevention &amp; control ; Ventricular tachycardia ; Voltage-Sensitive Dye Imaging</subject><ispartof>Toxicology and applied pharmacology, 2012-02, Vol.259 (1), p.66-73</ispartof><rights>2012 Elsevier Inc.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2012 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c413t-e88281428b882042ebf54128e8fd670c61510ee012e2c249e6ac5b8a2afa35b73</citedby><cites>FETCH-LOGICAL-c413t-e88281428b882042ebf54128e8fd670c61510ee012e2c249e6ac5b8a2afa35b73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=25642659$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22197715$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/22215241$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Jin-Bae</creatorcontrib><creatorcontrib>Kim, Changsoo</creatorcontrib><creatorcontrib>Choi, Eunmi</creatorcontrib><creatorcontrib>Park, Sanghoon</creatorcontrib><creatorcontrib>Park, Hyelim</creatorcontrib><creatorcontrib>Pak, Hui-Nam</creatorcontrib><creatorcontrib>Lee, Moon-Hyoung</creatorcontrib><creatorcontrib>Shin, Dong Chun</creatorcontrib><creatorcontrib>Hwang, Ki-Chul</creatorcontrib><creatorcontrib>Joung, Boyoung</creatorcontrib><title>Particulate air pollution induces arrhythmia via oxidative stress and calcium calmodulin kinase II activation</title><title>Toxicology and applied pharmacology</title><addtitle>Toxicol Appl Pharmacol</addtitle><description>Ambient particulate matter (PM) can increase the incidence of arrhythmia. 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DEP-induced APD prolongation, EAD and VT were successfully prevented with NAC (5mmol/L, n=5), nifedipine (10μmol/L, n=5), and active Ca2+/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. 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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 Ca2+/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. ► The ambient PM consistently prolonged repolarization. ► The ambient PM induced triggered activity and ventricular arrhythmia. ► These effects were prevented by antioxidants, ICaL blockade and CaMKII blockade. ► The ambient PM can induce arrhythmia via oxidative stress and activation of CaMKII.</abstract><cop>Amsterdam</cop><pub>Elsevier Inc</pub><pmid>22197715</pmid><doi>10.1016/j.taap.2011.12.007</doi><tpages>8</tpages></addata></record>
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identifier ISSN: 0041-008X
ispartof Toxicology and applied pharmacology, 2012-02, Vol.259 (1), p.66-73
issn 0041-008X
1096-0333
language eng
recordid cdi_osti_scitechconnect_22215241
source ScienceDirect Freedom Collection
subjects 60 APPLIED LIFE SCIENCES
Acetylcysteine - pharmacology
Action Potentials - drug effects
Air
Air Pollutants - toxicity
AIR POLLUTION
Animals
Animals, Newborn
ANTIOXIDANTS
APOPTOSIS
Apoptosis - drug effects
Arrhythmias, Cardiac - chemically induced
Arrhythmias, Cardiac - enzymology
Arrhythmias, Cardiac - metabolism
Arrhythmias, Cardiac - prevention & control
Biological and medical sciences
BIOLOGICAL STRESS
Ca2 +/calmodulin-dependent protein kinase II
CALCIUM
Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism
CALMODULIN
Cardiac dysrhythmias
Cardiology. Vascular system
Cells, Cultured
Dose-Response Relationship, Drug
Environmental pollutants toxicology
Enzyme Activation
HEART
Immunoblotting
Immunohistochemistry
IN VIVO
INFUSION
Male
Medical sciences
Myocytes, Cardiac - drug effects
Myocytes, Cardiac - metabolism
OXIDATION
Oxidative stress
Oxidative Stress - drug effects
OXYGEN
Particulate matter
Particulate Matter - toxicity
RATS
Rats, Sprague-Dawley
Reactive Oxygen Species - metabolism
Toxicology
Vehicle Emissions - toxicity
Ventricular fibrillation
Ventricular Premature Complexes - chemically induced
Ventricular Premature Complexes - enzymology
Ventricular Premature Complexes - metabolism
Ventricular Premature Complexes - prevention & control
Ventricular tachycardia
Voltage-Sensitive Dye Imaging
title Particulate air pollution induces arrhythmia via oxidative stress and calcium calmodulin kinase II activation
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