Ischemic preconditioning increases antioxidants in the brain and peripheral organs after cerebral ischemia

Background and purpose. Low molecular weight antioxidants (LMWA), which reflect tissue reducing power, are among the endogenous mechanisms for neutralizing reactive oxygen species (ROS). Ischemic preconditioning (IPC) was associated with decreased oxidative stress. We examined the effect of focal ischemia on LMWA and on prostaglandin E 2 (PGE 2, a product of arachidonic acid oxidation) in the brain, heart, liver, and lungs of rats subjected to 90 min of ischemia and in IPC rats subjected to similar insult. Methods. Transient right middle cerebral artery occlusion (MCAO) was performed for 90 min and at 0, 5, 30, 60, or 240 min of reperfusion, LMWA and PGE 2 were evaluated by cyclic voltametry (CV) and radioimmunoassay, respectively. IPC was induced by 2 min of MCAO, 24 h prior to the major ischemic episode. Results. LMWA decreased at 5 min of reperfusion in the brain, heart, liver, and lung and rose 4 h later only in the brain. PGE 2 levels increased three to fivefold in all tissues examined. Surprisingly, in IPC rats a dramatic increase of LMWA occurred at 5 min of reperfusion in the brain and in the peripheral organs. Uric acid, but not ascorbic, is the major LMWA increased. Conclusions. We propose that after ischemia, ROS rapidly consume the antioxidants reserves in the brain and also in peripheral organs, suggesting that the whole body is under oxidative stress. Moreover, part of the neuroprotection afforded by IPC is mediated by the brain's ability to mobilize antioxidants, especially uric acid, that attenuate the massive ROS-mediated oxidative stress

Grupos sociales y diversidad cultural. 65 Nueva Época (2002) enero-marzo. Antropología. Boletín Oficial del Instituto Nacional de Antropología e Historia

- Santa Claus en la hoguera por Claude Lévi-Strauss. - Semana Santa en Xoxocotla, Morelos. Cambios en la religiosidad popular por Luz María Brunt Rivera. - Adolescentes indígenas migrantes a la Ciudad de México por Ma. Sara Molinari Soriano y José Íñigo Aguilar Medina. - Mujeres de la Revolución en la obra del general Francisco L. Urquizo por Olga Cárdenas Trueba. - El lugar de los niños en la propuesta de educación socialista de México (1934-1940) por Ruth Guzik Glantz. - La Universidad Gabino Barreda (1934-1936) por Jesús Nieto Sotelo. - La elite política de la Ciudad de México en una época de transición por Lucio Ernesto Maldonado Ojeda. - Representaciones simbólicas del tiempo y el espacio entre los antiguos cholultecas por Sergio Suárez Cruz. - Apuntes para un análisis iconológico de los dioses navegantes en Izapa y Tikal por Emiliano Melgar Tísoc. - Santa Catalina y Santa Marina en la Pinacoteca del Museo de Guadalupe, Zacatecas por Alejandro Huerta Carrillo y Eugenia Berthier Villaseñor. - Pierre Bourdieu, una mirada de aprendiz por Selene Álvarez Larrauri. - Pierre Bourdieu: militante de la izquierda crítica y reflexiva por Jorge A. González. - El Museo Nacional en el imaginario mexicano por Salvador Rueda Smithers

Control of PKA stability and signalling by the RING ligase praja2

Activation of G-protein-coupled receptors (GPCRs) mobilizes compartmentalized pulses of cyclic AMP. The main cellular effector of cAMP is protein kinase A (PKA), which is assembled as an inactive holoenzyme consisting of two regulatory (R) and two catalytic (PKAc) subunits. cAMP binding to R subunits dissociates the holoenzyme and releases the catalytic moiety, which phosphorylates a wide array of cellular proteins. Reassociation of PKAc and R components terminates the signal. Here we report that the RING ligase praja2 controls the stability of mammalian R subunits. Praja2 forms a stable complex with, and is phosphorylated by, PKA. Rising cAMP levels promote praja2-mediated ubiquitylation and subsequent proteolysis of compartmentalized R subunits, leading to sustained substrate phosphorylation by the activated kinase. Praja2 is required for efficient nuclear cAMP signalling and for PKA-mediated long-term memory. Thus, praja2 regulates the total concentration of R subunits, tuning the strength and duration of PKA signal output in response to cAMP