title: [Role of mitochondria and reactive oxygen species in the progression of heart failure].
abstract: Congestive heart failure (CHF) would be associated with mitochondrial abnormalities and increased of reactive species of oxygen (ROS). To clarify these issues we studied the structure, function of the mitochondrial enzyme nitro oxide synthase inducible (iNOS) and lipoperoxidation of membranes, one of their products through the peroxide nitrite ion (ONOO-), in the heart muscle of patients with heart failure congestive (ICC) grade III and IV (according to New York Heart Association). We included 25 patients who underwent cardiovascular surgery to biopsies of the heart muscle. They were stratified into a group with CHF (n = 18) and control group (n = 7). In di-chas biopsies analyzed the enzymatic activity of mitochondrial complex III spectrophotometrically, which was measured in mM.ubiquinona-1.mg prot, while the mitochondrial morphology was analyzed by the Zeiss electron microscope, the areas were quantified with program Axionvision 4.6. Lipoperoxidation of membranes was measured by the presence of ONOO-by immunohistochemistry against primary antibody against 3-nitrotyrosine was used lab kit system biogenic steptobidin biotin peroxidase (SBA) and coloring triamiobencidina (TAB), it is made with semicuantificacion intensity SCORE test. The statistical test used was ANOVA. The heart muscle of patients with CHF showed that the mitochondrial area was reduced by 78% compared with the control (160.37 μm2 ± 9.87) (936.81 μm2 ± 78.48) p 0.0001. There was also a 70% reduction in complex III activity compared to control (1.9 10-2 mM ubiq.mim-prot 1.mg ± 12.6) (5.79 10-2mM ubiq.mim prot-1.mg ± 36.6) p . The presence of ONOO-was significantly increased in patients with CHF. Alterations ultraestructutural and functional mitochondria found in patients with CHF and increased ROS are involved in the measures of physiopathology CCI and whites should be taken into account for future therapies of this condition.
authors.affiliation: Cátedras de Física Biomédica, Histología y Microscopía Electrónica, Universidad Nacional de Córdoba, Sanatorio Allende y Clínica Aconcagua, Córdoba, Argentina.
authors.forename: Gustavo
authors.initials: G
authors.lastname: Guzman Mentesana
authors.forename: Alejandra
authors.initials: A
authors.lastname: Baez
authors.forename: Roque
authors.initials: R
authors.lastname: Córdoba
authors.forename: Ricardo
authors.initials: R
authors.lastname: Dominguez
authors.forename: Silvina
authors.initials: S
authors.lastname: Lo Presti
authors.forename: Walter
authors.initials: W
authors.lastname: Rivarola
authors.forename: Patricia
authors.initials: P
authors.lastname: Pons
authors.forename: Ricardo
authors.initials: R
authors.lastname: Fretes
authors.forename: Patricia
authors.initials: P
authors.lastname: Paglini-Oliva
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D018450:Disease Progression; D005260:Female; D006333:Heart Failure / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D046529:Microscopy, Electron, Transmission; D008929:Mitochondria, Heart / Q000502:physiology* / Q000648:ultrastructure; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism*; D012720:Severity of Illness Index; D014443:Tyrosine / Q000031:analogs & derivatives / Q000096:biosynthesis
chemical_list: D017382:Reactive Oxygen Species; C002744:3-nitrotyrosine; D014443:Tyrosine; D052247:Nitric Oxide Synthase Type II