IBIMOL   23987
INSTITUTO DE BIOQUIMICA Y MEDICINA MOLECULAR PROFESOR ALBERTO BOVERIS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Mitochondrial function in brain cortex and hippocampus of aged rats exposed to acute hypobaric hypoxia.
Autor/es:
KARADAYIAN, AG; LA PADULA, PH.; COSTA, LE.; CZERNICZYNIEC, A; LORES ARNAIZ, S
Lugar:
Mendoza
Reunión:
Simposio; II Simposio Internacional de Medicina Traslacional,; 2019
Institución organizadora:
Facultad de Ciencias Médicas, Centro universitario UNCuyo, Mendoza, Argentina
Resumen:
Mitochondrial function in brain cortex and hippocampus of aged rats exposed to acute hypobaric hypoxia.Czerniczyniec A1, La Padula P2, Karadayian A1, Lores Arnaiz S1, Costa LE21Instituto de Bioquímica y Medicina Molecular (UBA-CONICET), Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina 2Instituto de Investigaciones Cardiológicas ?Prof. Dr. Alberto C. Taquini?, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, ArgentinaIntroduction and objectives: Early results of our laboratory suggested that hippocampal and cortical mitochondria displayed different responses after exposure of animals during 1 or 7 months to hypobaric hypoxia (5000 m). The mechanisms responsible for acclimatization to chronic hypoxia would be time-dependent; nitric oxide metabolism and mitochondrial membrane potential changes would be successively involved as self-protective mechanisms in high altitude environment. The aim of the present work was to evaluate the effects of acute hypobaric hypoxia on cortical and hippocampal mitochondrial function in aged rats. Methods: Wistar rats (22 months) were exposed to 4400 m simulated altitude in a hypobaric chamber during 48 h. Oxygen consumption, mitochondrial membrane potential, UCP2 expression, nitric oxide and hydrogen peroxide production were evaluated in cortical and hippocampal mitochondria.Results: Cortical mitochondria from rats exposed to hypobaric hypoxia showed lower respiratory rates than controls in both states 4 (43%) and 3 (37%), and a decrease of mitochondrial membrane potential (19%). Mitochondrial NO and hydrogen peroxide production increased by 48%, and 23%, respectively. After acute hypobaric hypoxia, no significant changes were observed in oxygen consumption and hydrogen peroxide production in hippocampal mitochondria as compared with control animals. Mitochondrial membrane potential decreased (18%), whereas NO production increased by 46%, respectively.Conclusions: As well as showed previously during chronic acclimatization, in acute hypoxia hippocampal mitochondria display different responses than cortical mitochondria. Both tissues showed mild uncoupling and increased mitochondrial generation of NO, interpreted as self protective mechanisms against hypoxia. However, while hippocampus was able to preserve O2 consumption and H2O2 production, probably as compensation between both mechanisms, in cortical mitochondria those parameters were affected by hypoxia. At the same stimulus, biological systems would present different kind of strategies related to energy cell economy.