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http://repositorio.pediatria.gob.mx:8180/handle/20.500.12103/2709| Título : | Adrenaline stimulates H2O2 generation in liver via NADPH oxidase |
| Creador: | Díaz Cruz A., Guinzberg R., |
| Nivel de acceso: | Open access |
| Palabras clave : | Agonistas Adrenérgicos - farmacología Animales Membrana Celular - efectos de drogas Membrana Celular - metabolismo Activación Enzimática - efectos de drogas Epinefrina - farmacología Hepatocitos - citología Hepatocitos - efectos de drogas Hepatocitos - enzimología Peróxido de Hidrógeno - metabolismo Extractos Hepáticos - metabolismo Masculino NADPH Oxidasa - metabolismo Oxidantes - metabolismo Ratas Ratas Wistar Receptores Adrenérgicos - química Receptores Adrenérgicos - metabolismo Adrenergic Agonists - pharmacology Animals Cell Membrane - drug effects Cell Membrane - metabolism Enzyme Activation - drug effects Epinephrine - pharmacology Hepatocytes - cytology Hepatocytes - drug effects Hepatocytes - enzymology Hydrogen Peroxide - metabolism Liver Extracts - metabolism Male NADPH Oxidase - metabolism Oxidants - metabolism Rats Rats, Wistar Receptors, Adrenergic - chemistry Receptors, Adrenergic - metabolism Adrenaline Adrenergic receptors Hydrogen peroxide Liver cell membranes NADPH oxidase (Nox) ROS signaling |
| Descripción : | It is known that adrenaline promotes hydroxyl radical generation in isolated rat hepatocytes. The aim of this work was to investigate a potential role of NADPH oxidase (Nox) isoforms for an oxidative stress signal in response to adrenaline in hepatocytes. Enriched plasma membranes from isolated rat liver cells were prepared for this purpose. These membranes showed catalytic activity of Nox isoforms, probably Nox 2 based on its complete inhibition with specific antibodies. NADPH was oxidized to convert O2 into superoxide radical, later transformed into H2O2. This enzymatic activity requires previous activation with either 3mM Mn2+ or guanosine 5′-0-(3-thiotriphosphate) (GTPγS) plus adrenaline. Experimental conditions for activation and catalytic steps were set up: ATP was not required; S0.5 for NADPH was 44μM; S0.5 for FAD was 8μM; NADH up to 1mM was not substrate, and diphenyleneiodonium was inhibitory. Activation with GTPγS plus adrenaline was dose- and Ca2+-dependent and proceeded through α1-adrenergic receptors (AR), whereas β-AR stimulation resulted in inhibition of Nox activity. These results lead us to propose H2O2 as additional transduction signal for adrenaline response in hepatic cells. |
| Colaborador(es) u otros Autores: | Guerra R. Vilchis M. Carrasco D. García-Vázquez F.J. Piña E. |
| Fecha de publicación : | 2007 |
| Tipo de publicación: | Artículo |
| Formato: | |
| Identificador del Recurso : | 10.1080/10715760701268751 |
| Fuente: | Free Radical Research 41(6):663 - 672 |
| URI : | http://repositorio.pediatria.gob.mx:8180/handle/20.500.12103/2709 |
| Idioma: | eng |
| Aparece en las colecciones: | Artículos |
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