O6 Cardiac mitochondrial dysfunction time course in Type 1 Diabetes

Introduction: Results from our laboratory (Bombicino et al., 2016, 2017) have shown that sustained hyperglycemia for 25 days leads to generalized cardiac mitochondrial dysfunction that includes reduction of tissue and mitochondrial O2 consumption, complexes I-III, II-III and IV activities, ATP produ...

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Main Authors: Ivana Rukavina Mikusic, Micaela Rey, Manuela Martinefski, Valeria Trípodi, Laura Beatriz Valdez
Format: Article
Language:Spanish
Published: Sello Editorial Lugones 2020-11-01
Series:Revista de la Sociedad Argentina de Diabetes
Subjects:
Online Access:https://revistasad.com/index.php/diabetes/article/view/367
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author Ivana Rukavina Mikusic
Micaela Rey
Manuela Martinefski
Valeria Trípodi
Laura Beatriz Valdez
author_facet Ivana Rukavina Mikusic
Micaela Rey
Manuela Martinefski
Valeria Trípodi
Laura Beatriz Valdez
author_sort Ivana Rukavina Mikusic
collection DOAJ
description Introduction: Results from our laboratory (Bombicino et al., 2016, 2017) have shown that sustained hyperglycemia for 25 days leads to generalized cardiac mitochondrial dysfunction that includes reduction of tissue and mitochondrial O2 consumption, complexes I-III, II-III and IV activities, ATP production, ADP/O, and Mn-SOD activity; accompanied by enhancement of H2O2, NO and ONOO- generation rates, in addition to the triggering of mitochondrial biogenesis, although the "new" cardiac mitochondria of diabetic animals show structural alterations. This mitochondrial dysfunction occurs in the absence of hypertrophy and of changes in resting cardiac performance, but with cardiac compromise after a work overload, suggesting that mitochondrial dysfunction precedes myocardial failure in diabetic patients. Aim: To study the early events and to analyze the cardiac mitochondrial dysfunction time course in a type 1 Diabetes Mellitus model. Materials and methods: Diabetes was induced by Streptozotocin (STZ, single ip dose, 60 mg/kg) in male Wistar rats. Glycemia was measured at 72 h (C: 127 ± 5, DM: 415 ± 23 mg/dl). Animals were sacrificed 7, 10 or 14 days after STZ-injection (4, 7 or 11 days of hyperglycemia) and hearts were removed. Mitochondrial function and biogenesis, reactive oxygen and nitrogen species generation and redox state were determined
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spelling doaj.art-1c9dff77db694da9a8739bb2edbe79ff2022-12-22T03:43:27ZspaSello Editorial LugonesRevista de la Sociedad Argentina de Diabetes0325-52472346-94202020-11-01543Sup919110.47196/diab.v54i3Sup.367301O6 Cardiac mitochondrial dysfunction time course in Type 1 DiabetesIvana Rukavina Mikusic0Micaela Rey1Manuela Martinefski2Valeria Trípodi3Laura Beatriz Valdez4UNIVERSIDAD DE BUENOS AIRES, FACULTAD DE FARMACIA Y BIOQUÍMICA, FISICOQUÍMICA,INSTITUTO DE BIOQUIMICA Y MEDICINA MOLECULAR (IBIMOL), UNIVERSIDAD DE BUENOS AIRES, CONSEJO NACIONAL DE INVESTIGACIONES CIENTÍFICAS Y TÉCNICAS (UBA-CONICET), CIUDAD AUTÓNOMA DE BUENOS AIRES, ARGENTINAUNIVERSIDAD DE BUENOS AIRES, FACULTAD DE FARMACIA Y BIOQUÍMICA, FISICOQUÍMICA,CIUDAD AUTÓNOMA DE BUENOS AIRES, ARGENTINAUNIVERSIDAD DE BUENOS AIRES, FACULTAD DE FARMACIA Y BIOQUÍMICA, TECNOLOGÍA FARMACÉUTICA,CIUDAD AUTÓNOMA DE BUENOS AIRES, ARGENTINAUNIVERSIDAD DE BUENOS AIRES, FACULTAD DE FARMACIA Y BIOQUÍMICA, TECNOLOGÍA FARMACÉUTICA,CIUDAD AUTÓNOMA DE BUENOS AIRES, ARGENTINAUNIVERSIDAD DE BUENOS AIRES, FACULTAD DE FARMACIA Y BIOQUÍMICA, FISICOQUÍMICA,INSTITUTO DE BIOQUIMICA Y MEDICINA MOLECULAR (IBIMOL), UNIVERSIDAD DE BUENOS AIRES, CONSEJO NACIONAL DE INVESTIGACIONES CIENTÍFICAS Y TÉCNICAS (UBA-CONICET), CIUDAD AUTÓNOMA DE BUENOS AIRES, ARGENTINAIntroduction: Results from our laboratory (Bombicino et al., 2016, 2017) have shown that sustained hyperglycemia for 25 days leads to generalized cardiac mitochondrial dysfunction that includes reduction of tissue and mitochondrial O2 consumption, complexes I-III, II-III and IV activities, ATP production, ADP/O, and Mn-SOD activity; accompanied by enhancement of H2O2, NO and ONOO- generation rates, in addition to the triggering of mitochondrial biogenesis, although the "new" cardiac mitochondria of diabetic animals show structural alterations. This mitochondrial dysfunction occurs in the absence of hypertrophy and of changes in resting cardiac performance, but with cardiac compromise after a work overload, suggesting that mitochondrial dysfunction precedes myocardial failure in diabetic patients. Aim: To study the early events and to analyze the cardiac mitochondrial dysfunction time course in a type 1 Diabetes Mellitus model. Materials and methods: Diabetes was induced by Streptozotocin (STZ, single ip dose, 60 mg/kg) in male Wistar rats. Glycemia was measured at 72 h (C: 127 ± 5, DM: 415 ± 23 mg/dl). Animals were sacrificed 7, 10 or 14 days after STZ-injection (4, 7 or 11 days of hyperglycemia) and hearts were removed. Mitochondrial function and biogenesis, reactive oxygen and nitrogen species generation and redox state were determinedhttps://revistasad.com/index.php/diabetes/article/view/367disfunción mitocondrial cardíacaevolucióndiabetes tipo 1
spellingShingle Ivana Rukavina Mikusic
Micaela Rey
Manuela Martinefski
Valeria Trípodi
Laura Beatriz Valdez
O6 Cardiac mitochondrial dysfunction time course in Type 1 Diabetes
Revista de la Sociedad Argentina de Diabetes
disfunción mitocondrial cardíaca
evolución
diabetes tipo 1
title O6 Cardiac mitochondrial dysfunction time course in Type 1 Diabetes
title_full O6 Cardiac mitochondrial dysfunction time course in Type 1 Diabetes
title_fullStr O6 Cardiac mitochondrial dysfunction time course in Type 1 Diabetes
title_full_unstemmed O6 Cardiac mitochondrial dysfunction time course in Type 1 Diabetes
title_short O6 Cardiac mitochondrial dysfunction time course in Type 1 Diabetes
title_sort o6 cardiac mitochondrial dysfunction time course in type 1 diabetes
topic disfunción mitocondrial cardíaca
evolución
diabetes tipo 1
url https://revistasad.com/index.php/diabetes/article/view/367
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AT valeriatripodi o6cardiacmitochondrialdysfunctiontimecourseintype1diabetes
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