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Vitamin E Ameliorates the Decremental Effect of Paraquat on Cardiomyocyte Contractility in Rats
BACKGROUND: 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...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3601115/ https://www.ncbi.nlm.nih.gov/pubmed/23526948 http://dx.doi.org/10.1371/journal.pone.0057651 |
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author | Fahim, Mohamed Abdelmonem Howarth, Frank Christopher Nemmar, Abderrahim Qureshi, Mohamed Anwar Shafiullah, Mohamed Jayaprakash, Petrilla Hasan, Mohamed Yousif |
author_facet | Fahim, Mohamed Abdelmonem Howarth, Frank Christopher Nemmar, Abderrahim Qureshi, Mohamed Anwar Shafiullah, Mohamed Jayaprakash, Petrilla Hasan, Mohamed Yousif |
author_sort | Fahim, Mohamed Abdelmonem |
collection | PubMed |
description | BACKGROUND: 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. METHODOLOGY: 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. PRINCIPAL FINDINGS: 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. CONCLUSIONS: PAR exposure compromised rats heart function and ameliorated by vitamin E treatment. |
format | Online Article Text |
id | pubmed-3601115 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-36011152013-03-22 Vitamin E Ameliorates the Decremental Effect of Paraquat on Cardiomyocyte Contractility in Rats Fahim, Mohamed Abdelmonem Howarth, Frank Christopher Nemmar, Abderrahim Qureshi, Mohamed Anwar Shafiullah, Mohamed Jayaprakash, Petrilla Hasan, Mohamed Yousif PLoS One Research Article BACKGROUND: 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. METHODOLOGY: 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. PRINCIPAL FINDINGS: 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. CONCLUSIONS: PAR exposure compromised rats heart function and ameliorated by vitamin E treatment. Public Library of Science 2013-03-18 /pmc/articles/PMC3601115/ /pubmed/23526948 http://dx.doi.org/10.1371/journal.pone.0057651 Text en © 2013 Fahim et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Fahim, Mohamed Abdelmonem Howarth, Frank Christopher Nemmar, Abderrahim Qureshi, Mohamed Anwar Shafiullah, Mohamed Jayaprakash, Petrilla Hasan, Mohamed Yousif Vitamin E Ameliorates the Decremental Effect of Paraquat on Cardiomyocyte Contractility in Rats |
title | Vitamin E Ameliorates the Decremental Effect of Paraquat on Cardiomyocyte Contractility in Rats |
title_full | Vitamin E Ameliorates the Decremental Effect of Paraquat on Cardiomyocyte Contractility in Rats |
title_fullStr | Vitamin E Ameliorates the Decremental Effect of Paraquat on Cardiomyocyte Contractility in Rats |
title_full_unstemmed | Vitamin E Ameliorates the Decremental Effect of Paraquat on Cardiomyocyte Contractility in Rats |
title_short | Vitamin E Ameliorates the Decremental Effect of Paraquat on Cardiomyocyte Contractility in Rats |
title_sort | vitamin e ameliorates the decremental effect of paraquat on cardiomyocyte contractility in rats |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3601115/ https://www.ncbi.nlm.nih.gov/pubmed/23526948 http://dx.doi.org/10.1371/journal.pone.0057651 |
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