IBIMOL 23987
INSTITUTO DE BIOQUIMICA Y MEDICINA MOLECULAR PROFESOR ALBERTO BOVERIS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Mitochondrial NO and complex I syndrome in ischemia/reperfusion
Autor/es:
VALDEZ LB; ZAOBORNYJ T; BOMBICINO S; IGLESIAS DE; BOVERIS A; DONATO M; D'ANNUNZIO V; BUCHHOLZ B; GELPI R
Lugar:
La Plata
Reunión:
Congreso; XVIII Meeting of the International Society for Heart Research (ISHR), Latin American Section; 2010
Institución organizadora:
International Society for Heart Research (ISHR), Latin American Section
Resumen:
Isolated and perfused rabbit hearts were exposed to
ischemia and reperfusion (I: 15 min/R: 5 and 30 min). I/R decreased LV O2
consumption (46%) and malate-glutamate supported state 3 respiration (32%). Complex
I activity was 28% lower after I/R. Mitochondrial NO production decreased 28%,
with a diminished mtNOS
functional activity using malate-glutamate, and without modifications in mtNOS
expression. State 4 H2O2 production rate with
malate-glutamate was increased by 78% from control values after 30 min of
reperfusion. Mitochondrial phospholipid
oxidation products and mitochondrial protein tyrosine nitration were increased
by 42% and 50%, respectively, after I/R. The presence of adenosine in the perfusion solution attenuated
post-ischemic ventricular dysfunction and protected the tissue during I/R from
the declines of O2 consumption and complex I activity and from the
enhancement of mitochondrial phospholipid oxidation and tyrosine nitration. I/R
in the isolated rabbit heart leads to a condition of dysfunctional mitochondria, named complex I
syndrome, with decreased O2 uptake and complex I activity and with
increased H2O2 production, oxidation products content and
protein nitration. The beneficial effect of
adenosine could be attributed to preservation of tissue ATP levels associated
to a better regulation of the cardiomyocytes Ca2+ concentration.
