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

Marta Tajes, Gerard Ill-Raga, Ernest Palomer, Eva Ramos-Fernández, Francesc X. Guix, Mònica Bosch-Morató, Biuse Guivernau, Jordi Jiménez-Conde, Angel Ois, Fernando Pérez-Asensio, Mario Reyes-Navarro, Carolina Caballo, Ana M. Galán, Francesc Alameda, Ginés Escolar, Carlos Opazo, Anna Planas, Jaume Roquer, Miguel A. Valverde, Francisco J. Muñoz

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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.

Idioma originalAnglès
Número d’article826143
RevistaOxidative Medicine and Cellular Longevity
Estat de la publicacióPublicada - 2013
Publicat externament


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