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Nitro-oxidative stress after neuronal ischemia induces protein nitrotyrosination and cell death

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dc.contributor.author Tajes Orduña, Marta
dc.contributor.author Ill-Raga, Gerard, 1982-
dc.contributor.author Palomer, Ernest
dc.contributor.author Ramos Fernández, Eva, 1984-
dc.contributor.author Guix Ràfols, Francesc Xavier
dc.contributor.author Bosch Morató, Mònica, 1986-
dc.contributor.author Guivernau Almazán, Biuse, 1988-
dc.contributor.author Jiménez Conde, Jordi
dc.contributor.author Ois Santiago, Angel Javier
dc.contributor.author Pérez Asensio, Fernando
dc.contributor.author Reyes Navarro, Mario
dc.contributor.author Caballo, Carolina
dc.contributor.author Galán, Ana M.
dc.contributor.author Alameda Quitllet, Francisco
dc.contributor.author Escolar, Ginès
dc.contributor.author Opazo, Carlos M.
dc.contributor.author Planas, Anna
dc.contributor.author Roquer, Jaume
dc.contributor.author Valverde, M. A. (Miguel Ángel), 1963-
dc.contributor.author Muñoz López, Francisco José, 1964-
dc.date.accessioned 2015-12-02T19:27:58Z
dc.date.available 2015-12-02T19:27:58Z
dc.date.issued 2013
dc.identifier.citation Tajes M, Ill-Raga G, Palomer E, Ramos-Fernández E, Guix FX, Bosch-Morató M et al. Nitro-oxidative stress after neuronal ischemia induces protein nitrotyrosination and cell death. Oxid Med Cell Longev. 2013;2013:826143. DOI: 10.1155/2013/826143
dc.identifier.issn 1942-0900
dc.identifier.uri http://hdl.handle.net/10230/25318
dc.description.abstract Ischemic stroke is an acute vascular event that obstructs blood supply to the brain, producing irreversible damage that affects neurons but also glial and brain vessel cells. Immediately after the stroke, the ischemic tissue produces nitric oxide (NO) to recover blood perfusion but also produces superoxide anion. These compounds interact, producing peroxynitrite, which irreversibly nitrates protein tyrosines. The present study measured NO production in a human neuroblastoma (SH-SY5Y), a murine glial (BV2), a human endothelial cell line (HUVEC), and in primary cultures of human cerebral myocytes (HC-VSMCs) after experimental ischemia in vitro. Neuronal, endothelial, and inducible NO synthase (NOS) expression was also studied up to 24 h after ischemia, showing a different time course depending on the NOS type and the cells studied. Finally, we carried out cell viability experiments on SH-SY5Y cells with H2O2, a prooxidant agent, and with a NO donor to mimic ischemic conditions. We found that both compounds were highly toxic when they interacted, producing peroxynitrite. We obtained similar results when all cells were challenged with peroxynitrite. Our data suggest that peroxynitrite induces cell death and is a very harmful agent in brain ischemia.
dc.format.mimetype application/pdf
dc.language.iso eng
dc.publisher Hindawi
dc.relation.ispartof Oxidative medicine and cellular longevity. 2013; 2013: 826143
dc.rights © 2013 Tajes M et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
dc.rights.uri https://creativecommons.org/licenses/by/4.0/
dc.subject.other Estrès oxidatiu
dc.subject.other Proteïnes -- Metabolisme
dc.title Nitro-oxidative stress after neuronal ischemia induces protein nitrotyrosination and cell death
dc.type info:eu-repo/semantics/article
dc.identifier.doi http://dx.doi.org/10.1155/2013/826143
dc.rights.accessRights info:eu-repo/semantics/openAccess
dc.type.version info:eu-repo/semantics/publishedVersion


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