INQUIMAE   12526
INSTITUTO DE QUIMICA, FISICA DE LOS MATERIALES, MEDIOAMBIENTE Y ENERGIA
Unidad Ejecutora - UE
artículos
Título:
Effect of nitroxyl on the hamster retinal nitridergic pathway
Autor/es:
SAENZ, DANIEL A.; BARI, SARA E.; SALIDO, EZEQUIEL; CHIANELLI, M.; ROSENSTEIN, R.
Revista:
NEUROCHEMISTRY INTERNATIONAL
Editorial:
Elsevier
Referencias:
Año: 2007 vol. 51 p. 424 - 424
ISSN:
0197-0186
Resumen:
AbstractThere is a growing body of evidence on the role of nitric oxide (NO) in retinal physiology. Recently, interest has developed in the functional roleof an alternative redox form of NO, namely nitroxyl (HNO/NO), because it is formed by a number of diverse biochemical reactions. The aim ofthe present report was to comparatively analyze the effect of HNO and NO on the retinal nitridergic pathway in the golden hamster. For thispurpose, sodium trioxodinitrate (Angeli’s salt) and diethylammonium (Z)-1-(N,N-diethylamino)diazen-1-ium-1,2-diolate (DEA/NO) were used asHNO and NO releasers, respectively. Angeli’s salt and DEA/NO significantly decreased nitric oxide synthase activity. In addition, Angeli’s salt (butnot DEA/NO) significantly decreased L-arginine uptake. DEA/NO significantly increased cGMP accumulation at low micromolar concentrations,while Angeli’s salt affected this parameter with a threshold concentration of 200 mM. Although Angeli’s salt and DEA/NO significantlydiminished reduced glutathione and protein thiol levels in a similar way, DEA/NO was significantly more effective than AS in increasing Snitrosothiollevels. None of these compounds increased retinal lipid peroxidation. These results suggest that HNO could regulate the hamster retinalnitridergic pathway by acting through a mechanism that only partly overlaps with that involved in NO response.# 2007 Elsevier Ltd. All rights reserved.