| The role of oxidative stress in the development of congestive heart failure in a chicken genotype selected for rapid growth. | |
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MedLine Citation:
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PMID: 18622851 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The present study examined the possible role of reactive oxygen species in the pathogenesis of heart failure in broilers. Data were collected from three groups of birds at various risk of heart failure: Leghorn chickens (resistant to heart failure), slow-growing feed-restricted broilers (low risk of heart failure), fast-growing ad libitum fed broilers (high risk of heart failure), and broilers with congestive heart failure (CHF). In the first part of the study, basic clinical parameters and ultrastructural changes were examined in the context of lipid peroxidation of the ventricular myocardium. This was followed by the study of in vitro changes in the activity of selected cytosolic enzymes (creatine kinase and lactate dehydrogenase) and mitochondrial enzymes (pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase) in the presence of oxidants (hydrogen peroxide or tertiary butyl hydroperoxide). The distinctive clinical feature in the fast-growing broilers and in the broilers with CHF as compared with slow-growing broilers or Leghorn chickens was a significantly lower heart rate (P <0.05). Electron microscopy revealed marked morphological changes in myocardial mitochondria in these broilers (i.e. fast-growing broilers and broilers with CHF). The level of malondialdehyde equivalents, an indicator of lipid peroxidation subsequent to generated oxidative stress, was significantly higher (P <0.05) in ad libitum fed broilers and was highest (P <0.01) in broilers with CHF. In vitro, the presence of oxidants had a detrimental effect on creatine kinase and alpha-ketoglutarate dehydrogenase activity, while lactate dehydrogenase activity increased. The activity of pyruvate dehydrogenase was not altered by oxidants. Our results indicate that the deterioration of heart function in fast-growing commercial broilers in our experimental model is associated with oxidative stress leading to lipid peroxidation of cellular and mitochondrial membranes, and decreased activity of myocardial creatine kinase and alpha-ketoglutarate dehydrogenase enzymes critical for energy synthesis and transformation pathways. |
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Authors:
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S Nain; B Ling; B Bandy; J Alcorn; C Wojnarowicz; B Laarveld; A A Olkowski |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Avian pathology : journal of the W.V.P.A Volume: 37 ISSN: 1465-3338 ISO Abbreviation: Avian Pathol. Publication Date: 2008 Aug |
Date Detail:
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Created Date: 2008-07-14 Completed Date: 2008-10-27 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8210638 Medline TA: Avian Pathol Country: England |
Other Details:
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Languages: eng Pagination: 367-73 Citation Subset: IM |
Affiliation:
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Department of Animal and Poultry Science, University of Saskatchewan, Saskatoon, SK S7N 5A8, Canada. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Chickens / genetics*, growth & development* Food Deprivation Genetic Predisposition to Disease* Heart Failure / genetics, veterinary* Heart Rate Incidence Myocardium / enzymology Oxidative Stress / genetics* Poultry Diseases / genetics* |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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