Vitamin E ameliorates the decremental effect of paraquat on cardiomyocyte contractility in rats
Exposure to pesticides and industrial toxins are implicated in cardiovascular disease. Paraquat (PAR) is a toxic chemical widely used as an herbicide in developing countries and described as a major suicide agent. The hypothesis tested here is that PAR induced myocardial dysfunction may be attribute...
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| description | Exposure to pesticides and industrial toxins are implicated in cardiovascular disease. Paraquat (PAR) is a toxic chemical widely used as an herbicide in developing countries and described as a major suicide agent. The hypothesis tested here is that PAR induced myocardial dysfunction may be attributed to altered mechanisms of Ca(2+) transport which are in turn possibly linked to oxidative stress. The mechanisms of PAR induced myocardial dysfunction and the impact of antioxidant protection was investigated in rat ventricular myocytes.
Forty adult male Wistar rats were divided into 4 groups receiving the following daily intraperitoneal injections for 3 weeks: Group 1 PAR (10 mg/kg), Control Group 2 saline, Group 3 vitamin E (100 mg/kg) and Group 4 PAR (10 mg/kg) and vitamin E (100 mg/kg). Ventricular action potentials were measured in isolated perfused heart, shortening and intracellular Ca(2+) in electrically stimulated ventricular myocytes by video edge detection and fluorescence photometry techniques, and superoxide dismutase (SOD) and catalase (CAT) levels in heart tissue.
Spontaneous heart rate, resting cell length, time to peak (TPK) and time to half (THALF) relaxation of myocyte shortening were unaltered. Amplitude of shortening was significantly reduced in PAR treated rats (4.99±0.26%) and was normalized by vitamin E (7.46±0.44%) compared to controls (7.87±0.52%). PAR significantly increased myocytes resting intracellular Ca(2+) whilst TPK and THALF decay and amplitude of the Ca(2+) transient were unaltered. The fura-2-cell length trajectory during the relaxation of the twitch contraction was significantly altered in myocytes from PAR treated rats compared to controls suggesting altered myofilament sensitivity to Ca(2+) as it was normalized by vitamin E treatment. A significant increase in SOD and CAT activities was observed in both PAR and vitamin E plus PAR groups.
PAR exposure compromised rats heart function and ameliorated by vitamin E treatment. |
| doi_str_mv | 10.1371/journal.pone.0057651 |
| format | Article |
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Forty adult male Wistar rats were divided into 4 groups receiving the following daily intraperitoneal injections for 3 weeks: Group 1 PAR (10 mg/kg), Control Group 2 saline, Group 3 vitamin E (100 mg/kg) and Group 4 PAR (10 mg/kg) and vitamin E (100 mg/kg). Ventricular action potentials were measured in isolated perfused heart, shortening and intracellular Ca(2+) in electrically stimulated ventricular myocytes by video edge detection and fluorescence photometry techniques, and superoxide dismutase (SOD) and catalase (CAT) levels in heart tissue.
Spontaneous heart rate, resting cell length, time to peak (TPK) and time to half (THALF) relaxation of myocyte shortening were unaltered. Amplitude of shortening was significantly reduced in PAR treated rats (4.99±0.26%) and was normalized by vitamin E (7.46±0.44%) compared to controls (7.87±0.52%). PAR significantly increased myocytes resting intracellular Ca(2+) whilst TPK and THALF decay and amplitude of the Ca(2+) transient were unaltered. The fura-2-cell length trajectory during the relaxation of the twitch contraction was significantly altered in myocytes from PAR treated rats compared to controls suggesting altered myofilament sensitivity to Ca(2+) as it was normalized by vitamin E treatment. A significant increase in SOD and CAT activities was observed in both PAR and vitamin E plus PAR groups.
PAR exposure compromised rats heart function and ameliorated by vitamin E treatment.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0057651</identifier><identifier>PMID: 23526948</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Action Potentials - drug effects ; Agriculture ; Animals ; Antioxidants ; Biology ; Calcium (intracellular) ; Calcium ions ; Calcium Signaling - drug effects ; Calcium transport ; Cardiac muscle ; Cardiomyocytes ; Cardiovascular disease ; Cardiovascular diseases ; Catalase ; Catalase - metabolism ; Contractility ; Contraction ; Developing countries ; Drug dosages ; Edge detection ; Exposure ; Fatalities ; Fatty acids ; Fluorescence ; Free radicals ; Fura-2 ; Heart ; Heart function ; Heart rate ; Heart Rate - drug effects ; Herbicides ; Herbicides - antagonists & inhibitors ; Herbicides - toxicity ; In Vitro Techniques ; Intracellular ; Laboratory animals ; LDCs ; Male ; Medicine ; Muscle contraction ; Myocardial Contraction - drug effects ; Myocytes ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - physiology ; Oxidative stress ; Paraquat ; Paraquat - antagonists & inhibitors ; Paraquat - toxicity ; Parkinson's disease ; Parkinsons disease ; Pesticides ; Photometry ; Physiology ; Poisoning ; Public health ; Rats ; Rats, Wistar ; Rodents ; Smooth muscle ; Suicide ; Superoxide dismutase ; Superoxide Dismutase - metabolism ; Superoxides ; Tocopherol ; Toxicity ; Toxins ; Ventricle ; Vitamin E ; Vitamin E - pharmacology</subject><ispartof>PloS one, 2013-03, Vol.8 (3), p.e57651</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Fahim et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Fahim et al 2013 Fahim et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-5709338d67266494137ffa41f3e234c6aedd0939349f533e98d59f399f5c59173</citedby><cites>FETCH-LOGICAL-c692t-5709338d67266494137ffa41f3e234c6aedd0939349f533e98d59f399f5c59173</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3601115/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3601115/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79569,79570</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23526948$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fahim, Mohamed Abdelmonem</creatorcontrib><creatorcontrib>Howarth, Frank Christopher</creatorcontrib><creatorcontrib>Nemmar, Abderrahim</creatorcontrib><creatorcontrib>Qureshi, Mohamed Anwar</creatorcontrib><creatorcontrib>Shafiullah, Mohamed</creatorcontrib><creatorcontrib>Jayaprakash, Petrilla</creatorcontrib><creatorcontrib>Hasan, Mohamed Yousif</creatorcontrib><title>Vitamin E ameliorates the decremental effect of paraquat on cardiomyocyte contractility in rats</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Exposure to pesticides and industrial toxins are implicated in cardiovascular disease. Paraquat (PAR) is a toxic chemical widely used as an herbicide in developing countries and described as a major suicide agent. The hypothesis tested here is that PAR induced myocardial dysfunction may be attributed to altered mechanisms of Ca(2+) transport which are in turn possibly linked to oxidative stress. The mechanisms of PAR induced myocardial dysfunction and the impact of antioxidant protection was investigated in rat ventricular myocytes.
Forty adult male Wistar rats were divided into 4 groups receiving the following daily intraperitoneal injections for 3 weeks: Group 1 PAR (10 mg/kg), Control Group 2 saline, Group 3 vitamin E (100 mg/kg) and Group 4 PAR (10 mg/kg) and vitamin E (100 mg/kg). Ventricular action potentials were measured in isolated perfused heart, shortening and intracellular Ca(2+) in electrically stimulated ventricular myocytes by video edge detection and fluorescence photometry techniques, and superoxide dismutase (SOD) and catalase (CAT) levels in heart tissue.
Spontaneous heart rate, resting cell length, time to peak (TPK) and time to half (THALF) relaxation of myocyte shortening were unaltered. Amplitude of shortening was significantly reduced in PAR treated rats (4.99±0.26%) and was normalized by vitamin E (7.46±0.44%) compared to controls (7.87±0.52%). PAR significantly increased myocytes resting intracellular Ca(2+) whilst TPK and THALF decay and amplitude of the Ca(2+) transient were unaltered. The fura-2-cell length trajectory during the relaxation of the twitch contraction was significantly altered in myocytes from PAR treated rats compared to controls suggesting altered myofilament sensitivity to Ca(2+) as it was normalized by vitamin E treatment. A significant increase in SOD and CAT activities was observed in both PAR and vitamin E plus PAR groups.
PAR exposure compromised rats heart function and ameliorated by vitamin E treatment.</description><subject>Action Potentials - drug effects</subject><subject>Agriculture</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Biology</subject><subject>Calcium (intracellular)</subject><subject>Calcium ions</subject><subject>Calcium Signaling - drug effects</subject><subject>Calcium transport</subject><subject>Cardiac muscle</subject><subject>Cardiomyocytes</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular diseases</subject><subject>Catalase</subject><subject>Catalase - metabolism</subject><subject>Contractility</subject><subject>Contraction</subject><subject>Developing countries</subject><subject>Drug dosages</subject><subject>Edge detection</subject><subject>Exposure</subject><subject>Fatalities</subject><subject>Fatty acids</subject><subject>Fluorescence</subject><subject>Free radicals</subject><subject>Fura-2</subject><subject>Heart</subject><subject>Heart function</subject><subject>Heart rate</subject><subject>Heart Rate - drug effects</subject><subject>Herbicides</subject><subject>Herbicides - antagonists & inhibitors</subject><subject>Herbicides - toxicity</subject><subject>In Vitro Techniques</subject><subject>Intracellular</subject><subject>Laboratory animals</subject><subject>LDCs</subject><subject>Male</subject><subject>Medicine</subject><subject>Muscle contraction</subject><subject>Myocardial Contraction - drug effects</subject><subject>Myocytes</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - physiology</subject><subject>Oxidative stress</subject><subject>Paraquat</subject><subject>Paraquat - antagonists & inhibitors</subject><subject>Paraquat - toxicity</subject><subject>Parkinson's disease</subject><subject>Parkinsons disease</subject><subject>Pesticides</subject><subject>Photometry</subject><subject>Physiology</subject><subject>Poisoning</subject><subject>Public health</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Rodents</subject><subject>Smooth muscle</subject><subject>Suicide</subject><subject>Superoxide dismutase</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Superoxides</subject><subject>Tocopherol</subject><subject>Toxicity</subject><subject>Toxins</subject><subject>Ventricle</subject><subject>Vitamin E</subject><subject>Vitamin E - pharmacology</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl1r2zAUhs3YWD-2fzA2w6Cwi2SWZMvWTaGUbgsUCvvorTiRjhIF20oleSz_fsrilhg2GLrQkfScVzqvTpa9IcWcsJp83LjB99DOt67HeVFUNa_Is-yUCEZnnBbs-VF8kp2FsEkQazh_mZ1QVlEuyuY0k_c2Qmf7_CaHDlvrPEQMeVxjrlF57LCP0OZoDKqYO5NvwcPDACnucwVeW9ftnNpFzJXrowcVbWvjLk-SSSq8yl4YaAO-Hufz7Menm-_XX2a3d58X11e3M8UFjbOqLgRjjeY15bwUZarQGCiJYUhZqTig1okQrBSmYgxFoythmEgrVQlSs_Ps3UF327ogR2-CJIwVjWBFQROxOBDawUZuve3A76QDK_9sOL-S4KNVLUoN2ABrSqGWdakoWyICp5pwo-uGLzFpXY63DcsOtcJ95e1EdHrS27VcuZ-S8YIQUiWB96OAdw8DhviPJ4_UCtKrbG_c3uDOBiWvyrqhtCIFS9T8L1QaGjubPgWNTfuThA-ThP3H4a-4giEEufj29f_Zu_spe3HErhHauA6uHaJ1fZiC5QFU3oXg0Tw5Rwq5b-5HN-S-ueXY3Cnt7bHrT0mP3cx-A_ui9Lo</recordid><startdate>20130318</startdate><enddate>20130318</enddate><creator>Fahim, Mohamed Abdelmonem</creator><creator>Howarth, Frank Christopher</creator><creator>Nemmar, Abderrahim</creator><creator>Qureshi, Mohamed Anwar</creator><creator>Shafiullah, Mohamed</creator><creator>Jayaprakash, Petrilla</creator><creator>Hasan, Mohamed Yousif</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PIMPY</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20130318</creationdate><title>Vitamin E ameliorates the decremental effect of paraquat on cardiomyocyte contractility in rats</title><author>Fahim, Mohamed Abdelmonem ; Howarth, Frank Christopher ; Nemmar, Abderrahim ; Qureshi, Mohamed Anwar ; Shafiullah, Mohamed ; Jayaprakash, Petrilla ; Hasan, Mohamed Yousif</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-5709338d67266494137ffa41f3e234c6aedd0939349f533e98d59f399f5c59173</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Action Potentials - 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Paraquat (PAR) is a toxic chemical widely used as an herbicide in developing countries and described as a major suicide agent. The hypothesis tested here is that PAR induced myocardial dysfunction may be attributed to altered mechanisms of Ca(2+) transport which are in turn possibly linked to oxidative stress. The mechanisms of PAR induced myocardial dysfunction and the impact of antioxidant protection was investigated in rat ventricular myocytes.
Forty adult male Wistar rats were divided into 4 groups receiving the following daily intraperitoneal injections for 3 weeks: Group 1 PAR (10 mg/kg), Control Group 2 saline, Group 3 vitamin E (100 mg/kg) and Group 4 PAR (10 mg/kg) and vitamin E (100 mg/kg). Ventricular action potentials were measured in isolated perfused heart, shortening and intracellular Ca(2+) in electrically stimulated ventricular myocytes by video edge detection and fluorescence photometry techniques, and superoxide dismutase (SOD) and catalase (CAT) levels in heart tissue.
Spontaneous heart rate, resting cell length, time to peak (TPK) and time to half (THALF) relaxation of myocyte shortening were unaltered. Amplitude of shortening was significantly reduced in PAR treated rats (4.99±0.26%) and was normalized by vitamin E (7.46±0.44%) compared to controls (7.87±0.52%). PAR significantly increased myocytes resting intracellular Ca(2+) whilst TPK and THALF decay and amplitude of the Ca(2+) transient were unaltered. The fura-2-cell length trajectory during the relaxation of the twitch contraction was significantly altered in myocytes from PAR treated rats compared to controls suggesting altered myofilament sensitivity to Ca(2+) as it was normalized by vitamin E treatment. A significant increase in SOD and CAT activities was observed in both PAR and vitamin E plus PAR groups.
PAR exposure compromised rats heart function and ameliorated by vitamin E treatment.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23526948</pmid><doi>10.1371/journal.pone.0057651</doi><tpages>e57651</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2013-03, Vol.8 (3), p.e57651 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1330893002 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Action Potentials - drug effects Agriculture Animals Antioxidants Biology Calcium (intracellular) Calcium ions Calcium Signaling - drug effects Calcium transport Cardiac muscle Cardiomyocytes Cardiovascular disease Cardiovascular diseases Catalase Catalase - metabolism Contractility Contraction Developing countries Drug dosages Edge detection Exposure Fatalities Fatty acids Fluorescence Free radicals Fura-2 Heart Heart function Heart rate Heart Rate - drug effects Herbicides Herbicides - antagonists & inhibitors Herbicides - toxicity In Vitro Techniques Intracellular Laboratory animals LDCs Male Medicine Muscle contraction Myocardial Contraction - drug effects Myocytes Myocytes, Cardiac - drug effects Myocytes, Cardiac - physiology Oxidative stress Paraquat Paraquat - antagonists & inhibitors Paraquat - toxicity Parkinson's disease Parkinsons disease Pesticides Photometry Physiology Poisoning Public health Rats Rats, Wistar Rodents Smooth muscle Suicide Superoxide dismutase Superoxide Dismutase - metabolism Superoxides Tocopherol Toxicity Toxins Ventricle Vitamin E Vitamin E - pharmacology |
| title | Vitamin E ameliorates the decremental effect of paraquat on cardiomyocyte contractility in rats |
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