IBIMOL   23987
INSTITUTO DE BIOQUIMICA Y MEDICINA MOLECULAR PROFESOR ALBERTO BOVERIS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Nitric oxide metabolism and apoptosis due to after-effects of acute ethanol exposure in brain cortex.
Autor/es:
BUSTAMANTE, J.; CZERNICZYNIEC, A.; KARADAYIAN, A.G.; LORES ARNAIZ, S.
Lugar:
Mar del Plata
Reunión:
Congreso; LXIV Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC),; 2019
Institución organizadora:
Sociedad Argentina de Investigación Clínica
Resumen:
Acute alcohol consumption involves huge quantities of alcohol consumed in a short period of time. Thus, alcohol? after-effects, known as alcohol hangover (AH) is defined as the combination of mental and physical symptoms experienced the day after a single episode of heavy drinking, starting when blood alcohol concentration approaches zero. We previously evidenced bioenergetics alterations and oxidative stress in synaptosomes. The aim of the present work was to study nitric oxide (NO) metabolism and mitochondrial apoptotic markers. Mice received an i.p. injection of ethanol (3.8 g/kg body weight, AH group) or saline (control group) and were sacrificed 6 h afterwards (hangover onset). Brain cortex synaptosomes and mitochondria crude fraction were obtained by differential Ficoll gradient and differential centrifugation, respectively. Methods included the determination of NOS activity by spectrophotometry, total content of NO by flow cytometry, expression of neuronal- and inducible- NOS isoforms and expression of PSD95 and the NR2B-subunit of NMDAR by Western blot analysis. Mitochondrial apoptotic markers included the analysis of mitochondrial permeability transition (MPT) and the expression of Bax and Bcl-2 together with the analysis of cytochrome c release from mitochondria to cytosol by Western blot. Results raised from synaptosomes showed a 37% decrease in total content of NO (p