IBIMOL   23987
INSTITUTO DE BIOQUIMICA Y MEDICINA MOLECULAR PROFESOR ALBERTO BOVERIS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Pancreatic mitochondrial bioenergetics in an animal model of acute pancreatitis
Autor/es:
VANASCO VIRGINIA; MARCHINI TIMOTEO; MAGNANI NATALIA; ALVAREZ SILVIA; VACCARO MARÍA INÉS
Lugar:
Buenos Aires
Reunión:
Conferencia; Conferences Buenos Aires 2013 Autophagy: Biology and Disease; 2013
Institución organizadora:
Facultad de Farmacia y Bioquímica - CONICET
Resumen:
An
alteration in the autophagic flux or a defect in the selective autophagy of
secretory granules (zymophagy) during Acute pancreatitis (AP), promotes cell
damage and the progression to a severe disease (JBC 2011). ATP and other
molecules necessary in autophagy process are provided by mitochondria, so a
normal mitochondrial bioenergetics would be necessary for maintaining the
autophagic process in response to the disease. The aim of this study was to
analyze mitochondrial bioenergetics and its relationship with the autophagic
process in an experimental model of severe AP. Female Sprague-Dawley rats (45 days
old) were ip injected with caerulein (CAE) 50 mg/kg ip 1h intervals. Treated
groups were studied: CAE 1, animals injected with a single dose and then
sacrificed 1h; CAE 3, animals injected with 3 doses and sacrificed at 3h; CAE
24, animals injected with 6 doses and sacrificed at 24 h. Simultaneously with
each CAE group, control groups (CG) were performed using the same protocol but
injected with vehicle. CAE 3 and CAE 24 animals show mitochondrial O2
consumption in state 3 decreased by 30 and 40% respectively (CG: 40 ± 5
ng-atO/min.mg prot). These results are reflected in a decrease in mitochondrial
respiratory control. ATP production was observed for all CAE groups decreased,
and this difference was greater in CAE3 group (CG: 140 ± 18 nmol ATP/ min.mg.prot,
P < 0.01). These results demonstrate that mitochondrial bioenergetic profile
is impaired early during experimental AP, which may affect zymography flux
leading to the cell damage characteristic of the severe disease.