IBIMOL   23987
INSTITUTO DE BIOQUIMICA Y MEDICINA MOLECULAR PROFESOR ALBERTO BOVERIS
Unidad Ejecutora - UE
artículos
Título:
Complex I syndrome and nitric oxide in rabbit heart in ischemia-reperfusion. Effect of adenosine
Autor/es:
VALDEZ LB; ZAOBORNYJ T; BOMBICINO SS; IGLESIAS DE; DONATO M; D´ANNUNZIO V; BOVERIS A; GELPI R
Revista:
FREE RADICAL BIOLOGY AND MEDICINE
Editorial:
ELSEVIER SCIENCE INC
Referencias:
Año: 2011 vol. 51 p. 1203 - 1212
ISSN:
0891-5849
Resumen:
Isolated rabbit hearts were exposed to ischemia (I: 15 min) and reperfusion (R: 5-30 min) as a model of stunned myocardium. I/R decreased left ventricle O2 consumption (46%) and malate-glutamate supported mitochondrial state 3 respiration (32%). Activities of complex I, but not of complexes II and IV, were 28% lower after I/R. The pattern observed for the decline of complex I activity was also observed for the reduction of mtNOS biochemical (28%) and functional activities, in accordance to the reported physical and functional interaction between complex I and mtNOS. Malate-glutamate supported state 4 H2O2 production was increased by 78% after I/R. Mn-SOD activity (53 ± 5 USOD/mg protein) and concentration (7.4 ± 0.7 M) were not modified by I/R. Mitochondrial phospholipid oxidation products were increased by 42%, whereas protein oxidation was only slightly increased. I/R produced a marked (50%) enhancement in tyrosine nitration of the mitochondrial proteins. Adenosine attenuated post-ischemic ventricular dysfunction and protected the tissue from the declines of O2 consumption and of complex I and mtNOS activities and from the enhancement of mitochondrial phospholipid oxidation. Rabbit myocardial stunning leads to a condition of dysfunctional mitochondria named “complex I syndrome”. The beneficial effect of adenosine could be attributed to a better regulation of intracellular cardiomyocyte Ca2+ concentration.