Effect of nitroxyl on the hamster retinal nitridergic pathway

There is a growing body of evidence on the role of nitric oxide (NO) in retinal physiology. Recently, interest has developed in the functional role of an alternative redox form of NO, namely nitroxyl (HNO/NO-), because it is formed by a number of diverse biochemical reactions. The aim of the present...

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Autor principal: Sáenz, D.A
Otros Autores: Bari, S.E, Salido, E., Chianelli, M., Rosenstein, R.E
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: 2007
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245 1 0 |a Effect of nitroxyl on the hamster retinal nitridergic pathway 
260 |c 2007 
270 1 0 |m Rosenstein, R.E.; Laboratorio de Neuroquímica Retiniana y Oftalmología Experimental, Departamento de Bioquímica Humana, Facultad de Medicina, Buenos Aires, Argentina; email: ruthr@fmed.uba.ar 
506 |2 openaire  |e Política editorial 
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520 3 |a There is a growing body of evidence on the role of nitric oxide (NO) in retinal physiology. Recently, interest has developed in the functional role of an alternative redox form of NO, namely nitroxyl (HNO/NO-), because it is formed by a number of diverse biochemical reactions. The aim of the present report was to comparatively analyze the effect of HNO and NO on the retinal nitridergic pathway in the golden hamster. For this purpose, sodium trioxodinitrate (Angeli's salt) and diethylammonium (Z)-1-(N,N-diethylamino)diazen-1-ium-1,2-diolate (DEA/NO) were used as HNO and NO releasers, respectively. Angeli's salt and DEA/NO significantly decreased nitric oxide synthase activity. In addition, Angeli's salt (but not 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 μM. Although Angeli's salt and DEA/NO significantly diminished reduced glutathione and protein thiol levels in a similar way, DEA/NO was significantly more effective than AS in increasing S-nitrosothiol levels. None of these compounds increased retinal lipid peroxidation. These results suggest that HNO could regulate the hamster retinal nitridergic pathway by acting through a mechanism that only partly overlaps with that involved in NO response. © 2007 Elsevier Ltd. All rights reserved.  |l eng 
536 |a Detalles de la financiación: Universidad de Buenos Aires 
536 |a Detalles de la financiación: Agencia Nacional de Promoción Científica y Tecnológica 
536 |a Detalles de la financiación: Consejo Nacional de Investigaciones Científicas y Técnicas 
536 |a Detalles de la financiación: This research was supported by grants from the Agencia Nacional de Promoción Científica y Tecnológica (ANPCyT), University of Buenos Aires, and CONICET. 
593 |a Laboratorio de Neuroquímica Retiniana y Oftalmología Experimental, Departamento de Bioquímica Humana, Facultad de Medicina, Buenos Aires, Argentina 
593 |a Departamento de Química Inorgánica, Analítica y Química Física/INQUIMAE, Facultad de Ciencias Exactas y Naturales, Buenos Aires, Argentina 
690 1 0 |a NITRIC OXIDE 
690 1 0 |a NITROXYL 
690 1 0 |a RETINA 
690 1 0 |a AMINE 
690 1 0 |a AMMONIUM DERIVATIVE 
690 1 0 |a ARGININE 
690 1 0 |a CYCLIC GMP 
690 1 0 |a DIETHYLAMMONIUM 1 (N,N DIETHYLAMINO)DIAZEN 1 IUM 1,2 DIOLATE 
690 1 0 |a GLUTATHIONE 
690 1 0 |a NITRIC ACID DERIVATIVE 
690 1 0 |a NITRIC OXIDE 
690 1 0 |a NITRIC OXIDE SYNTHASE 
690 1 0 |a NITROXYL 
690 1 0 |a S NITROSOTHIOL 
690 1 0 |a SODIUM DERIVATIVE 
690 1 0 |a SODIUM TRIOXODINITRATE 
690 1 0 |a THIOL 
690 1 0 |a UNCLASSIFIED DRUG 
690 1 0 |a ANIMAL CELL 
690 1 0 |a ANIMAL TISSUE 
690 1 0 |a ARTICLE 
690 1 0 |a COMPARATIVE STUDY 
690 1 0 |a CONCENTRATION (PARAMETERS) 
690 1 0 |a CONTROLLED STUDY 
690 1 0 |a ENZYME ACTIVITY 
690 1 0 |a LIPID PEROXIDATION 
690 1 0 |a MALE 
690 1 0 |a NONHUMAN 
690 1 0 |a OXIDATION REDUCTION POTENTIAL 
690 1 0 |a PRIORITY JOURNAL 
690 1 0 |a REGULATORY MECHANISM 
690 1 0 |a RETINA NERVE CELL 
690 1 0 |a SYRIAN HAMSTER 
690 1 0 |a ANIMALS 
690 1 0 |a ANTIOXIDANTS 
690 1 0 |a ARGININE 
690 1 0 |a CRICETINAE 
690 1 0 |a CYCLIC GMP 
690 1 0 |a DOSE-RESPONSE RELATIONSHIP, DRUG 
690 1 0 |a GLUTATHIONE 
690 1 0 |a LIPID PEROXIDATION 
690 1 0 |a MALE 
690 1 0 |a MESOCRICETUS 
690 1 0 |a NITRERGIC NEURONS 
690 1 0 |a NITRIC OXIDE 
690 1 0 |a NITRIC OXIDE SYNTHASE 
690 1 0 |a NITRITES 
690 1 0 |a NITROGEN OXIDES 
690 1 0 |a OXIDATIVE STRESS 
690 1 0 |a QUATERNARY AMMONIUM COMPOUNDS 
690 1 0 |a RETINA 
690 1 0 |a S-NITROSOTHIOLS 
690 1 0 |a SIGNAL TRANSDUCTION 
690 1 0 |a VISUAL PATHWAYS 
690 1 0 |a CRICETINAE 
690 1 0 |a MESOCRICETUS AURATUS 
700 1 |a Bari, S.E. 
700 1 |a Salido, E. 
700 1 |a Chianelli, M. 
700 1 |a Rosenstein, R.E. 
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