| Cardiac oxidative stress is involved in heart failure induced by thiamine deprivation in rats. | |
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MedLine Citation:
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PMID: 20304817 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Thiamine is an important cofactor of metabolic enzymes, and its deficiency leads to cardiovascular dysfunction. First, we characterized the metabolic status measuring resting oxygen consumption rate and lactate blood concentration after 35 days of thiamine deficiency (TD). The results pointed to a decrease in resting oxygen consumption and a twofold increase in blood lactate. Confocal microscopy showed that intracellular superoxide (approximately 40%) and H(2)O(2) (2.5 times) contents had been increased. In addition, biochemical activities and protein expression of SOD, glutathione peroxidase, and catalase were evaluated in hearts isolated from rats submitted to thiamine deprivation. No difference in SOD activity was detected, but protein levels were found to be increased. Catalase activity increased 2.1 times in TD hearts. The observed gain in activity was attended by an increased catalase protein level. However, a marked decrease in glutathione peroxidase activity (control 435.3 + or - 28.6 vs. TD 199.4 + or - 30.2 nmol NADPH x min(-1) x ml(-1)) was paralleled by a diminution in the protein levels. Compared with control hearts, we did observe a greater proportion of apoptotic myocytes by TdT-mediated dUTP nick end labeling (TUNEL) and caspase-3 reactivity techniques. These results indicate that during TD, reactive oxygen species (ROS) production may be enhanced as a consequence of the installed acidosis. The perturbation in the cardiac myocytes redox balance was responsible for the increase in apoptosis. |
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Authors:
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Carolina Rosa Gioda; Tatiane de Oliveira Barreto; Thales Nicolau Pr?mola-Gomes; Daniel Carvalho de Lima; Paula Peixoto Campos; Luciano dos Santos Aggunn Capettini; Sandra Lauton-Santos; Anilton C?sar Vasconcelos; C?ndido C Coimbra; Virginia Soares Lemos; Jorge L Pesquero; Jader S Cruz |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-03-19 |
Journal Detail:
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Title: American journal of physiology. Heart and circulatory physiology Volume: 298 ISSN: 1522-1539 ISO Abbreviation: Am. J. Physiol. Heart Circ. Physiol. Publication Date: 2010 Jun |
Date Detail:
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Created Date: 2010-05-20 Completed Date: 2010-06-23 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100901228 Medline TA: Am J Physiol Heart Circ Physiol Country: United States |
Other Details:
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Languages: eng Pagination: H2039-45 Citation Subset: IM |
Affiliation:
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Dept. of Biochemistry and Immunology, Federal Univ. of Minas Gerais, Belo Horizonte, MG 31270-090, Brazil. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis / physiology Catalase / metabolism Disease Models, Animal Glutathione Peroxidase / metabolism Heart / physiopathology* Heart Failure / etiology*, physiopathology* Lactates / blood Male Myocardium / metabolism, pathology Oxidative Stress / physiology* Oxygen Consumption / physiology Rats Rats, Wistar Reactive Oxygen Species / metabolism Superoxide Dismutase / metabolism Thiamine Deficiency / complications* |
| Chemical | |
Reg. No./Substance:
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0/Lactates; 0/Reactive Oxygen Species; EC 1.11.1.6/Catalase; EC 1.11.1.9/Glutathione Peroxidase; EC 1.15.1.1/Superoxide Dismutase |
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