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Iron induces protection and necrosis in cultured cardiomyocytes: Role of reactive oxygen species and nitric oxide

Authordc.contributor.authorMuñoz, Juan Pablo 
Authordc.contributor.authorChiong Lay, Mario es_CL
Authordc.contributor.authorGarcía Nannig, Lorena es_CL
Authordc.contributor.authorTroncoso Cotal, Rodrigo es_CL
Authordc.contributor.authorToro, Barbra es_CL
Authordc.contributor.authorPedrozo Cibils, Zully es_CL
Authordc.contributor.authorDíaz Elizondo, Jessica es_CL
Authordc.contributor.authorSalas, Daniela es_CL
Authordc.contributor.authorParra Ortíz, María Valentina es_CL
Authordc.contributor.authorNúñez González, Marco es_CL
Authordc.contributor.authorHidalgo Tapia, María Cecilia es_CL
Authordc.contributor.authorLavandero González, Sergio es_CL
Cita de ítemdc.identifier.citationFREE RADICAL BIOLOGY AND MEDICINE 48 (4): 526-534en_US
Abstractdc.description.abstractWe investigate here the role of reactive oxygen species and nitric oxide in iron-induced cardiomyocyte hypertrophy or cell death Cultured rat cardiomyocytes incubated with 20 mu M iron (added as FeCl3-Na nitrilotriacetate, Fe-NTA) displayed hypertrophy features that: included increased protein synthesis and cell size, plus realignment of F-actin filaments along with sarcomeres and activation of the atrial natriuretic factor acne promoter Incubation with higher Fe-NTA concentrations (100 mu M) produced cardiomyocyte death,by necrosis. Incubation for 24 h with Fe-NTA (20-40 mu M) or the nitric oxide donor Delta-nonoate increased iNOS mRNA but decreased iNOS protein levels: under these conditions. Lion stimulated the activity and the dimerization of iNOS. Fe-NTA (20 mu M) promoted short- and long-term generation of reactive oxygen species, whereas preincubation with L-arginine suppressed this response Preincubation with 20 mu M Fe-NTA also attenuated the necrotic cell death triggered by 100 mu M Fe-NTA, suggesting that these preincubation conditions have cardioprotective effects Inhibition of iNOS activity with 1400 W enhanced Iron-induced ROS generation and prevented both iron-dependent cardiomyocyte hypertrophy and cardioprotection In conclusion. we propose that Fe-NTA (20 mu M) stimulates iNOs activity and that the enhanced NO production, by promoting hypertrophy and enhancing survival mechanisms through ROS reduction, is beneficial to cardiomyocytes. At higher concentrations, however, iron triggers cardiomyocyte death by necrosis.en_US
Publisherdc.publisherELSEVIER SCIENCE INCen_US
Títulodc.titleIron induces protection and necrosis in cultured cardiomyocytes: Role of reactive oxygen species and nitric oxideen_US
Document typedc.typeArtículo de revistaen_US

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