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Biochemical Studies on the Cardioprotective Effect of Glutamine on Tissue Antioxidant Defense System in Isoprenaline-Induced Myocardial Infarction in Rats
Oxidative stress is one of the mechanisms with a central role involved in the pathogenesis of myocardial infarction. The protective effect of glutamine on myocardial antioxidant defense system was investigated during isoprenaline-induced myocardial infarction, an animal model of myocardial infarctio...
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Formato: | Texto |
Lenguaje: | English |
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the Society for Free Radical Research Japan
2007
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2291504/ https://www.ncbi.nlm.nih.gov/pubmed/18437213 http://dx.doi.org/10.3164/jcbn.40.49 |
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author | H.S. Kumar, Subramaniam Anandan, Rangasamy |
author_facet | H.S. Kumar, Subramaniam Anandan, Rangasamy |
author_sort | H.S. Kumar, Subramaniam |
collection | PubMed |
description | Oxidative stress is one of the mechanisms with a central role involved in the pathogenesis of myocardial infarction. The protective effect of glutamine on myocardial antioxidant defense system was investigated during isoprenaline-induced myocardial infarction, an animal model of myocardial infarction of human beings. Levels of diagnostic marker enzymes in plasma, reduced glutathione (GSH) and lipid peroxides and the activities of glutathione peroxidase, glutathione-S-transferase, catalase and superoxide dismutase in heart tissue were determined. Injection of isoprenaline caused significant increases in the levels of diagnostic marker enzymes in plasma and lipid peroxidation in heart tissue. A parallel decline in the levels of ATP (Adenosine triphosphate) and GSH and the activities of glutathione-dependent antioxidant enzymes and antiperoxidative enzymes in heart tissue was also observed. Prior oral administration of glutamine significantly prevented isoprenaline-induced adverse effects and maintained myocardial antioxidant status at near normal status. The cardioprotective effect of glutamine is probably related to a strengthening of the myocardial membrane by its membrane stabilizing action, or to a counteraction of free radicals by its antioxidant property, or to its ability to maintain near to normal status the activities of free radical scavenging enzymes and the level of GSH, which protect myocardial membrane against oxidative damage by decreasing lipid peroxidation. |
format | Text |
id | pubmed-2291504 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2007 |
publisher | the Society for Free Radical Research Japan |
record_format | MEDLINE/PubMed |
spelling | pubmed-22915042008-04-24 Biochemical Studies on the Cardioprotective Effect of Glutamine on Tissue Antioxidant Defense System in Isoprenaline-Induced Myocardial Infarction in Rats H.S. Kumar, Subramaniam Anandan, Rangasamy J Clin Biochem Nutr Original Article Oxidative stress is one of the mechanisms with a central role involved in the pathogenesis of myocardial infarction. The protective effect of glutamine on myocardial antioxidant defense system was investigated during isoprenaline-induced myocardial infarction, an animal model of myocardial infarction of human beings. Levels of diagnostic marker enzymes in plasma, reduced glutathione (GSH) and lipid peroxides and the activities of glutathione peroxidase, glutathione-S-transferase, catalase and superoxide dismutase in heart tissue were determined. Injection of isoprenaline caused significant increases in the levels of diagnostic marker enzymes in plasma and lipid peroxidation in heart tissue. A parallel decline in the levels of ATP (Adenosine triphosphate) and GSH and the activities of glutathione-dependent antioxidant enzymes and antiperoxidative enzymes in heart tissue was also observed. Prior oral administration of glutamine significantly prevented isoprenaline-induced adverse effects and maintained myocardial antioxidant status at near normal status. The cardioprotective effect of glutamine is probably related to a strengthening of the myocardial membrane by its membrane stabilizing action, or to a counteraction of free radicals by its antioxidant property, or to its ability to maintain near to normal status the activities of free radical scavenging enzymes and the level of GSH, which protect myocardial membrane against oxidative damage by decreasing lipid peroxidation. the Society for Free Radical Research Japan 2007-01 2006-12-27 /pmc/articles/PMC2291504/ /pubmed/18437213 http://dx.doi.org/10.3164/jcbn.40.49 Text en Copyright © 2006 JCBN This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article H.S. Kumar, Subramaniam Anandan, Rangasamy Biochemical Studies on the Cardioprotective Effect of Glutamine on Tissue Antioxidant Defense System in Isoprenaline-Induced Myocardial Infarction in Rats |
title | Biochemical Studies on the Cardioprotective Effect of Glutamine on Tissue Antioxidant Defense System in Isoprenaline-Induced Myocardial Infarction in Rats |
title_full | Biochemical Studies on the Cardioprotective Effect of Glutamine on Tissue Antioxidant Defense System in Isoprenaline-Induced Myocardial Infarction in Rats |
title_fullStr | Biochemical Studies on the Cardioprotective Effect of Glutamine on Tissue Antioxidant Defense System in Isoprenaline-Induced Myocardial Infarction in Rats |
title_full_unstemmed | Biochemical Studies on the Cardioprotective Effect of Glutamine on Tissue Antioxidant Defense System in Isoprenaline-Induced Myocardial Infarction in Rats |
title_short | Biochemical Studies on the Cardioprotective Effect of Glutamine on Tissue Antioxidant Defense System in Isoprenaline-Induced Myocardial Infarction in Rats |
title_sort | biochemical studies on the cardioprotective effect of glutamine on tissue antioxidant defense system in isoprenaline-induced myocardial infarction in rats |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2291504/ https://www.ncbi.nlm.nih.gov/pubmed/18437213 http://dx.doi.org/10.3164/jcbn.40.49 |
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