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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 |
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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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► 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 & 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</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&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. 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><subject>60 APPLIED LIFE SCIENCES</subject><subject>Acetylcysteine - pharmacology</subject><subject>Action Potentials - drug effects</subject><subject>Air</subject><subject>Air Pollutants - toxicity</subject><subject>AIR POLLUTION</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>ANTIOXIDANTS</subject><subject>APOPTOSIS</subject><subject>Apoptosis - drug effects</subject><subject>Arrhythmias, Cardiac - chemically induced</subject><subject>Arrhythmias, Cardiac - enzymology</subject><subject>Arrhythmias, Cardiac - metabolism</subject><subject>Arrhythmias, Cardiac - prevention & control</subject><subject>Biological and medical sciences</subject><subject>BIOLOGICAL STRESS</subject><subject>Ca2 +/calmodulin-dependent protein kinase II</subject><subject>CALCIUM</subject><subject>Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism</subject><subject>CALMODULIN</subject><subject>Cardiac dysrhythmias</subject><subject>Cardiology. Vascular system</subject><subject>Cells, Cultured</subject><subject>Dose-Response Relationship, Drug</subject><subject>Environmental pollutants toxicology</subject><subject>Enzyme Activation</subject><subject>HEART</subject><subject>Immunoblotting</subject><subject>Immunohistochemistry</subject><subject>IN VIVO</subject><subject>INFUSION</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>OXIDATION</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>OXYGEN</subject><subject>Particulate matter</subject><subject>Particulate Matter - toxicity</subject><subject>RATS</subject><subject>Rats, Sprague-Dawley</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Toxicology</subject><subject>Vehicle Emissions - toxicity</subject><subject>Ventricular fibrillation</subject><subject>Ventricular Premature Complexes - chemically induced</subject><subject>Ventricular Premature Complexes - enzymology</subject><subject>Ventricular Premature Complexes - metabolism</subject><subject>Ventricular Premature Complexes - prevention & control</subject><subject>Ventricular tachycardia</subject><subject>Voltage-Sensitive Dye Imaging</subject><issn>0041-008X</issn><issn>1096-0333</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><recordid>eNp9kU-LFDEQxYMo7jj6BTxIQBZP3abS_8GLLKsOLLgHBW-hOl3NZOxOxiQ9uN9-08yoNw-hAvnVq7x6jL0GkYOA-v0hj4jHXAqAHGQuRPOEbUB0dSaKonjKNkKUkAnR_rhiL0I4CCG6soTn7EpK6JoGqg2b79FHo5cJI3E0nh_dNC3ROMuNHRZNgaP3-4e4nw3yUzrutxkwmhPxED2F9G4HrnHSZpnXOrthmYzlP43FQHy346gTjqvmS_ZsxCnQq0vdsu-fbr_dfMnuvn7e3Xy8y3QJRcyobWULpWz7dBGlpH6sSpAtteNQN0LXUIEgEiBJall2VKOu-hYljlhUfVNs2duzrgvRqKBNJL3XzlrSUcnkvpJp0Ja9O1NH734tFKKaTdA0TWjJLUF1Mml30HWJlGdSexeCp1EdvZnRPygQas1CHdSahVqzUCBVyiI1vbnIL_1Mw9-WP8tPwPUFwJAWN3q02oR_XFWXsq7W6R_OHKWVnQz51RFZTYPxq6HBmf_94xGHOqhQ</recordid><startdate>20120215</startdate><enddate>20120215</enddate><creator>Kim, Jin-Bae</creator><creator>Kim, Changsoo</creator><creator>Choi, Eunmi</creator><creator>Park, Sanghoon</creator><creator>Park, Hyelim</creator><creator>Pak, Hui-Nam</creator><creator>Lee, Moon-Hyoung</creator><creator>Shin, Dong Chun</creator><creator>Hwang, Ki-Chul</creator><creator>Joung, Boyoung</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>OTOTI</scope></search><sort><creationdate>20120215</creationdate><title>Particulate air pollution induces arrhythmia via oxidative stress and calcium calmodulin kinase II activation</title><author>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</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c413t-e88281428b882042ebf54128e8fd670c61510ee012e2c249e6ac5b8a2afa35b73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>60 APPLIED LIFE SCIENCES</topic><topic>Acetylcysteine - pharmacology</topic><topic>Action Potentials - drug effects</topic><topic>Air</topic><topic>Air Pollutants - toxicity</topic><topic>AIR POLLUTION</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>ANTIOXIDANTS</topic><topic>APOPTOSIS</topic><topic>Apoptosis - drug effects</topic><topic>Arrhythmias, Cardiac - chemically induced</topic><topic>Arrhythmias, Cardiac - enzymology</topic><topic>Arrhythmias, Cardiac - metabolism</topic><topic>Arrhythmias, Cardiac - prevention & control</topic><topic>Biological and medical sciences</topic><topic>BIOLOGICAL STRESS</topic><topic>Ca2 +/calmodulin-dependent protein kinase II</topic><topic>CALCIUM</topic><topic>Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism</topic><topic>CALMODULIN</topic><topic>Cardiac dysrhythmias</topic><topic>Cardiology. Vascular system</topic><topic>Cells, Cultured</topic><topic>Dose-Response Relationship, Drug</topic><topic>Environmental pollutants toxicology</topic><topic>Enzyme Activation</topic><topic>HEART</topic><topic>Immunoblotting</topic><topic>Immunohistochemistry</topic><topic>IN VIVO</topic><topic>INFUSION</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>OXIDATION</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>OXYGEN</topic><topic>Particulate matter</topic><topic>Particulate Matter - toxicity</topic><topic>RATS</topic><topic>Rats, Sprague-Dawley</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Toxicology</topic><topic>Vehicle Emissions - toxicity</topic><topic>Ventricular fibrillation</topic><topic>Ventricular Premature Complexes - chemically induced</topic><topic>Ventricular Premature Complexes - enzymology</topic><topic>Ventricular Premature Complexes - metabolism</topic><topic>Ventricular Premature Complexes - prevention & control</topic><topic>Ventricular tachycardia</topic><topic>Voltage-Sensitive Dye Imaging</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><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><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>OSTI.GOV</collection><jtitle>Toxicology and applied pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Jin-Bae</au><au>Kim, Changsoo</au><au>Choi, Eunmi</au><au>Park, Sanghoon</au><au>Park, Hyelim</au><au>Pak, Hui-Nam</au><au>Lee, Moon-Hyoung</au><au>Shin, Dong Chun</au><au>Hwang, Ki-Chul</au><au>Joung, Boyoung</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Particulate air pollution induces arrhythmia via oxidative stress and calcium calmodulin kinase II activation</atitle><jtitle>Toxicology and applied pharmacology</jtitle><addtitle>Toxicol Appl Pharmacol</addtitle><date>2012-02-15</date><risdate>2012</risdate><volume>259</volume><issue>1</issue><spage>66</spage><epage>73</epage><pages>66-73</pages><issn>0041-008X</issn><eissn>1096-0333</eissn><coden>TXAPA9</coden><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 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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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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