Mitochondrial function in rat brain cortex and hippocampus after long term hypobaric hypoxia

CZERNICZYNIEC, A; LORES ARNAIZ, S; BUSTAMANTE, J.; LA PADULA, PH.; COSTA, LE.

Congreso; VIII Meeting of the Society of Free Radical Biology and Medicine South American Group; 2013

Mitochondrial function in rat brain cortex and hippocampus after long term hypobaric hypoxia Czerniczyniec A.1, Lores Arnaiz S.1, Bustamante J.1 , La Padula P.2, Costa LE.2   1 Instituto de Bioquímica y Medicina Molecular, Facultad de Farmacia y Bioquímica and  2Instituto de Investigaciones Cardiológicas, Facultad de Medicina, UBA-CONICET   Mitochondria isolated from hippocampus of rats submitted to hypobaric hypoxia for 1 month showed an increase in nitric oxide synthase expression along with a decrease in O2 consumption. In the present study mitochondrial function in brain of rats submitted to prolonged hypoxia was analyzed. Mitochondrial fraction was isolated from brain cortex and hippocampus of rats exposed to 53.8 kPa in a hipopressure chamber for 7 months (HH), and their controls (C) at 101.3 kPa. Nitric oxide production, determined by the spectrophotometric method of the oxyhemoglobin and O2 consumption, measured by a high resolution respirometer, were unchanged. Membrane depolarization, evaluated by flow citometry, increased (%) from 13.7 ± 1.2 to 25.6 ± 2.5 (p<0.001) in hippocampus and from 10.6 ± 0.5 to 17.4 ± 1.2 (p<0.05) in cortex. Hydrogen peroxide production, determined by the scopoletin-HRP procedure, tended to decrease (12%) in cortex and (20%) in hippocampus. It is concluded that the protective mechanism previously described is not observed after a prolonged period of relatively severe hypoxia. However, results may be interpreted within the frame of the hypothesis "uncoupling to survive" (Brand, 2000), whereby a moderate fall in membrane potential would decrease reactive oxygen species generation and the consequent oxidative damage. PIP1688/09.