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However, beside this protector effect, high NO concentrations produce neuronal death by a mechanism in which the caspase pathway is implicated. In this work, we demonstrate that in cortical neurons the NO toxicity is mediated by mitochondrial dysfunction. SNAP, an NO donor, induces apoptosis in these cells because it 1) increases the p53 and 2) induces cytochrome c release and activation of caspase\u20109 and caspase\u20103. SNAP also induces necrosis, through 1) breakdown of the mitochondrial membrane potential, 2) ATP decrease, 3) ROS formation, and 4) LDH and ATP release, indicative of oxidative stress and death by necrosis. To sum up, in cortical neurons, high NO concentrations produced cellular death by both an apoptotic and a necrotic mechanism in which the mitochondria are implicated. \u00a9 2006 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.20739","type":"journal-article","created":{"date-parts":[[2006,1,6]],"date-time":"2006-01-06T00:20:06Z","timestamp":1136506806000},"page":"441-449","source":"Crossref","is-referenced-by-count":47,"title":["Mitochondrial involvement in nitric oxide\u2010induced cellular death in cortical neurons in 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