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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 presen...
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Published in: | Neurochemistry international 2007-11, Vol.51 (6), p.424-432 |
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description | 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. |
doi_str_mv | 10.1016/j.neuint.2007.04.015 |
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−), 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.</description><identifier>ISSN: 0197-0186</identifier><identifier>EISSN: 1872-9754</identifier><identifier>DOI: 10.1016/j.neuint.2007.04.015</identifier><identifier>PMID: 17543420</identifier><identifier>CODEN: NEUIDS</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Animals ; Antioxidants - pharmacology ; Arginine - metabolism ; Biological and medical sciences ; Cricetinae ; Cyclic GMP - metabolism ; Dose-Response Relationship, Drug ; Eye and associated structures. Visual pathways and centers. Vision ; Fundamental and applied biological sciences. Psychology ; Glutathione - drug effects ; Glutathione - metabolism ; Lipid Peroxidation - drug effects ; Lipid Peroxidation - physiology ; Male ; Mesocricetus ; Nitrergic Neurons - metabolism ; Nitric oxide ; Nitric Oxide - metabolism ; Nitric Oxide - pharmacology ; Nitric Oxide Synthase - drug effects ; Nitric Oxide Synthase - metabolism ; Nitrites - pharmacology ; Nitrogen Oxides - metabolism ; Nitrogen Oxides - pharmacology ; Nitroxyl ; Oxidative Stress - drug effects ; Oxidative Stress - physiology ; Quaternary Ammonium Compounds - pharmacology ; Retina ; Retina - drug effects ; Retina - metabolism ; S-Nitrosothiols - metabolism ; Signal Transduction - drug effects ; Signal Transduction - physiology ; Vertebrates: nervous system and sense organs ; Visual Pathways - drug effects ; Visual Pathways - metabolism</subject><ispartof>Neurochemistry international, 2007-11, Vol.51 (6), p.424-432</ispartof><rights>2007 Elsevier Ltd</rights><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c436t-63568381041651c0cd658a2f9d3a8eebe381b8fd5dbecadb810719d4d32b44d33</citedby><cites>FETCH-LOGICAL-c436t-63568381041651c0cd658a2f9d3a8eebe381b8fd5dbecadb810719d4d32b44d33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19158610$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17543420$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sáenz, Daniel A.</creatorcontrib><creatorcontrib>Bari, Sara E.</creatorcontrib><creatorcontrib>Salido, Ezequiel</creatorcontrib><creatorcontrib>Chianelli, Mónica</creatorcontrib><creatorcontrib>Rosenstein, Ruth E.</creatorcontrib><title>Effect of nitroxyl on the hamster retinal nitridergic pathway</title><title>Neurochemistry international</title><addtitle>Neurochem Int</addtitle><description>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.</description><subject>Animals</subject><subject>Antioxidants - pharmacology</subject><subject>Arginine - metabolism</subject><subject>Biological and medical sciences</subject><subject>Cricetinae</subject><subject>Cyclic GMP - metabolism</subject><subject>Dose-Response Relationship, Drug</subject><subject>Eye and associated structures. Visual pathways and centers. Vision</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Glutathione - drug effects</subject><subject>Glutathione - metabolism</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Lipid Peroxidation - physiology</subject><subject>Male</subject><subject>Mesocricetus</subject><subject>Nitrergic Neurons - metabolism</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide - pharmacology</subject><subject>Nitric Oxide Synthase - drug effects</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Nitrites - pharmacology</subject><subject>Nitrogen Oxides - metabolism</subject><subject>Nitrogen Oxides - pharmacology</subject><subject>Nitroxyl</subject><subject>Oxidative Stress - drug effects</subject><subject>Oxidative Stress - physiology</subject><subject>Quaternary Ammonium Compounds - pharmacology</subject><subject>Retina</subject><subject>Retina - drug effects</subject><subject>Retina - metabolism</subject><subject>S-Nitrosothiols - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - physiology</subject><subject>Vertebrates: nervous system and sense organs</subject><subject>Visual Pathways - drug effects</subject><subject>Visual Pathways - metabolism</subject><issn>0197-0186</issn><issn>1872-9754</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><recordid>eNp9kMtOwzAQRS0EgvL4A4SygV3COLGdZAESqspDQmIDa8uxJ9RVmhTbBfr3uDQSOzYzi3vmanQIOaeQUaDiepH1uLZ9yHKAMgOWAeV7ZEKrMk_rkrN9MgFalynQShyRY-8XEMEa-CE5ojEvWA4TcjNrW9QhGdqkt8EN35suGfokzDGZq6UP6BKHwfaq-82tQfdudbJSYf6lNqfkoFWdx7Nxn5C3-9nr9DF9fnl4mt49p5oVIqSi4KIqKgqMCk41aCN4pfK2NoWqEBuMWVO1hpsGtTJNJEtaG2aKvGFxFifkate7csPHGn2QS-s1dp3qcVh7GdsFQM0jyHagdoP3Dlu5cnap3EZSkFttciF32uRWmwQmo7Z4djH2r5slmr-j0VMELkdAea261qleW__H1ZRXgm652x2H0canRSe9tthrNNZFzdIM9v9PfgB1y40V</recordid><startdate>20071101</startdate><enddate>20071101</enddate><creator>Sáenz, Daniel A.</creator><creator>Bari, Sara E.</creator><creator>Salido, Ezequiel</creator><creator>Chianelli, Mónica</creator><creator>Rosenstein, Ruth E.</creator><general>Elsevier Ltd</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20071101</creationdate><title>Effect of nitroxyl on the hamster retinal nitridergic pathway</title><author>Sáenz, Daniel A. ; Bari, Sara E. ; Salido, Ezequiel ; Chianelli, Mónica ; Rosenstein, Ruth E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c436t-63568381041651c0cd658a2f9d3a8eebe381b8fd5dbecadb810719d4d32b44d33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Antioxidants - pharmacology</topic><topic>Arginine - metabolism</topic><topic>Biological and medical sciences</topic><topic>Cricetinae</topic><topic>Cyclic GMP - metabolism</topic><topic>Dose-Response Relationship, Drug</topic><topic>Eye and associated structures. Visual pathways and centers. Vision</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Glutathione - drug effects</topic><topic>Glutathione - metabolism</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Lipid Peroxidation - physiology</topic><topic>Male</topic><topic>Mesocricetus</topic><topic>Nitrergic Neurons - metabolism</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide - pharmacology</topic><topic>Nitric Oxide Synthase - drug effects</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Nitrites - pharmacology</topic><topic>Nitrogen Oxides - metabolism</topic><topic>Nitrogen Oxides - pharmacology</topic><topic>Nitroxyl</topic><topic>Oxidative Stress - drug effects</topic><topic>Oxidative Stress - physiology</topic><topic>Quaternary Ammonium Compounds - pharmacology</topic><topic>Retina</topic><topic>Retina - drug effects</topic><topic>Retina - metabolism</topic><topic>S-Nitrosothiols - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - physiology</topic><topic>Vertebrates: nervous system and sense organs</topic><topic>Visual Pathways - drug effects</topic><topic>Visual Pathways - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sáenz, Daniel A.</creatorcontrib><creatorcontrib>Bari, Sara E.</creatorcontrib><creatorcontrib>Salido, Ezequiel</creatorcontrib><creatorcontrib>Chianelli, Mónica</creatorcontrib><creatorcontrib>Rosenstein, Ruth E.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Neurochemistry international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sáenz, Daniel A.</au><au>Bari, Sara E.</au><au>Salido, Ezequiel</au><au>Chianelli, Mónica</au><au>Rosenstein, Ruth E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of nitroxyl on the hamster retinal nitridergic pathway</atitle><jtitle>Neurochemistry international</jtitle><addtitle>Neurochem Int</addtitle><date>2007-11-01</date><risdate>2007</risdate><volume>51</volume><issue>6</issue><spage>424</spage><epage>432</epage><pages>424-432</pages><issn>0197-0186</issn><eissn>1872-9754</eissn><coden>NEUIDS</coden><abstract>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.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>17543420</pmid><doi>10.1016/j.neuint.2007.04.015</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Antioxidants - pharmacology Arginine - metabolism Biological and medical sciences Cricetinae Cyclic GMP - metabolism Dose-Response Relationship, Drug Eye and associated structures. Visual pathways and centers. Vision Fundamental and applied biological sciences. Psychology Glutathione - drug effects Glutathione - metabolism Lipid Peroxidation - drug effects Lipid Peroxidation - physiology Male Mesocricetus Nitrergic Neurons - metabolism Nitric oxide Nitric Oxide - metabolism Nitric Oxide - pharmacology Nitric Oxide Synthase - drug effects Nitric Oxide Synthase - metabolism Nitrites - pharmacology Nitrogen Oxides - metabolism Nitrogen Oxides - pharmacology Nitroxyl Oxidative Stress - drug effects Oxidative Stress - physiology Quaternary Ammonium Compounds - pharmacology Retina Retina - drug effects Retina - metabolism S-Nitrosothiols - metabolism Signal Transduction - drug effects Signal Transduction - physiology Vertebrates: nervous system and sense organs Visual Pathways - drug effects Visual Pathways - metabolism |
title | Effect of nitroxyl on the hamster retinal nitridergic pathway |
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