Apoptosis and necrosis: two distinct events induced, respectively, by mild and intense insults with N-methyl-D-aspartate or nitric oxide/superoxide in cortical cell cultures

摘要: Abstract N-Methyl-D-aspartate (NMDA) receptor-mediated neurotoxicity may depend, in part, on the generation of nitric oxide (NO.) and superoxide anion (O2.-), which react to form peroxynitrite (OONO-). This is thought contribute a final common pathway injury wide variety acute chronic neurologic disorders, including focal ischemia, trauma, epilepsy, Huntington disease, Alzheimer amyotrophic lateral scelerosis, AIDS dementia, other neurodegenerative diseases. Here, we report that exposure cortical neurons relatively short durations or low concentrations NMDA, S-nitrosocysteine, 3-morpholinosydnonimine, generate levels peroxynitrite, induces delayed predominated by apoptotic features. Pretreatment with dismutase catalase scavenge O2.- partially prevents process triggered S-nitrosocysteine 3-morpholinosydnonimine. In contrast, intense high NMDA necrotic cell damage characterized swelling lysis, cannot be ameliorated catalase. Thus, depending intensity initial insult, oxide/superoxide can result either neuronal damage.