© 2000 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
Mitochondrial function in heart muscle from patients with idiopathic dilated cardiomyopathy
aGrup dInvestigació Muscular, Departament de Medicina, Hospital Clinic i Provincial, IDIBAPS, Facultat de Medicina, UB, Villarroel 170, 08036 Barcelona, Spain
bServei de Cardiologia, Institut de Malalties Cardiovasculars, Hospital Clinic i Provincial, Barcelona, Spain
cDepartment of Neurology and Cell Biology and Anatomy, University of Miami, School of Medicine, Miami, FL, USA
* Corresponding author. Tel.: +34-93-227-5539; fax: +34-93-227-5539 jordi{at}medicina.ub.es
Objective: To study the mitochondrial respiratory chain enzyme activities in patients with idiopathic dilated cardiomyopathy (IDC). Methods: Mitochondrial respiratory chain enzyme activities were assessed spectrophotometrically in left ventricular tissue of 17 patients with IDC undergoing cardiac transplantation, as well as in two groups of controls: a group of six patients suffering from ischemic dilated cardiomyopathy (IC) also undergoing cardiac transplantation, and a group of 17 organ donors considered normal from a cardiac point of view. Cytochrome b gene from three IDC patients whose complex III activity was particularly low and from three controls was also sequenced. Results: We found that complex III enzymatic activity was lower not only in IDC but also in IC patients when compared with normal controls. When analysing cytochrome b gene we only found neutral polymorphisms previously described. Conclusions: In view of such results, we believe that the decrease of respiratory chain complex III activity found in some cases of IDC is a secondary phenomenon, and not due to a primary mitochondrial disease.
KEYWORDS Cardiomyopathy; Energy metabolism; Gene therapy; Mitochondria; Oxidative phosphorylation
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
X. Gao, J. L. Campian, M. Qian, X.-F. Sun, and J. W. Eaton Mitochondrial DNA Damage in Iron Overload J. Biol. Chem., February 20, 2009; 284(8): 4767 - 4775. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. G. Rosca, E. J. Vazquez, J. Kerner, W. Parland, M. P. Chandler, W. Stanley, H. N. Sabbah, and C. L. Hoppel Cardiac mitochondria in heart failure: decrease in respirasomes and oxidative phosphorylation Cardiovasc Res, October 1, 2008; 80(1): 30 - 39. [Abstract] [Full Text] [PDF] |
||||

