| Cortical and hippocampal mitochondria bioenergetics and oxidative status during hyperglycemia and/or insulin-induced hypoglycemia. | |
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MedLine Citation:
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PMID: 20620209 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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This study was undertaken to evaluate the effects of streptozotocin (STZ)-induced hyperglycemia and insulin-induced hypoglycemia in cortical and hippocampal mitochondria bioenergetics and oxidative status. For that purpose we used, citrate (vehicle)-treated Wistar rats, STZ-treated rats [i.p., 50mg/kg body weight] and STZ-treated rats injected with insulin [s.c., dose adjusted to blood glucose levels] 1h prior to sacrifice to induce an acute episode of hypoglycemia. Several parameters were analyzed: respiratory chain, phosphorylation system, thiobarbituric acid reactive substances (TBARS) levels, hydrogen peroxide (H(2)O(2)) production rate, and non-enzymatic and enzymatic antioxidant defenses. Cortical mitochondria from insulin-induced hypoglycemic rats present a significant decrease in the ADP/O index, a significant increase in the repolarization lag phase and a decrease in GSH/GSSG ratio when compared with STZ and control mitochondria. Both STZ-induced diabetes and insulin-induced hypoglycemia promote a significant increase in TBARS levels and a decrease in glutathione disulfide reductase activity. Diabetic cortical mitochondria present a significant decrease in glutathione peroxidase (GPx) activity compared to control mitochondria. In turn, insulin-induced hypoglycemia induced a significant increase in GPx and manganese superoxide dismutase (MnSOD) activities. In hippocampal mitochondria, insulin-induced hypoglycemia increases the respiratory control ratio whereas both situations, hyper- and hypoglycemia, potentiate H(2)O(2) production and decrease the activity of MnSOD. These results suggest that the poor glycemic control that occurs in type 1 diabetic patients undergoing insulin therapy may have detrimental effects in brain areas involved in learning and memory. |
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Authors:
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Susana Cardoso; Maria S Santos; Raquel Seiça; Paula I Moreira |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-07-08 |
Journal Detail:
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Title: Biochimica et biophysica acta Volume: 1802 ISSN: 0006-3002 ISO Abbreviation: Biochim. Biophys. Acta Publication Date: 2010 Nov |
Date Detail:
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Created Date: 2010-09-20 Completed Date: 2010-12-10 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0217513 Medline TA: Biochim Biophys Acta Country: Netherlands |
Other Details:
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Languages: eng Pagination: 942-51 Citation Subset: IM |
Copyright Information:
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Copyright © 2010 Elsevier B.V. All rights reserved. |
Affiliation:
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Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517 Coimbra, Portugal. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Blood Glucose / metabolism Cerebral Cortex / metabolism* Diabetes Mellitus, Experimental / blood, chemically induced, metabolism Energy Metabolism Glutathione / metabolism Glutathione Disulfide / metabolism Glutathione Peroxidase / metabolism Hemoglobin A, Glycosylated / metabolism Hippocampus / metabolism* Hyperglycemia / blood, chemically induced, metabolism* Insulin Male Membrane Potential, Mitochondrial Mitochondria / metabolism* Oxidation-Reduction Oxidative Phosphorylation Rats Rats, Wistar Reactive Oxygen Species / metabolism Streptozocin Superoxide Dismutase / metabolism Thiobarbituric Acid Reactive Substances / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Blood Glucose; 0/Hemoglobin A, Glycosylated; 0/Reactive Oxygen Species; 0/Thiobarbituric Acid Reactive Substances; 11061-68-0/Insulin; 18883-66-4/Streptozocin; 27025-41-8/Glutathione Disulfide; 70-18-8/Glutathione; EC 1.11.1.9/Glutathione Peroxidase; EC 1.15.1.1/Superoxide Dismutase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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