Hydrogen peroxide cytotoxicity in cultured cardiac myocytes is iron dependent.
Am J Physiol
; 266(1 Pt 2): H121-7, 1994 Jan.
Article
en En
| MEDLINE
| ID: mdl-8304492
Because of its potential importance in injury during myocardial ischemia and reperfusion, we assessed mechanisms of hydrogen peroxide (H2O2) cytotoxicity in cultured chick embryo cardiac myocytes. Injury was quantitated by release of lactate dehydrogenase (LDH) or 51Cr, both of which correlated with loss of cell viability assessed by trypan blue exclusion. The iron chelator deferoxamine (0.25-2 mM), but not equimolar iron-loaded deferoxamine, markedly reduced LDH and 51Cr release. Injury was also prevented or attenuated by the diffusible reactive oxygen metabolite scavengers dimethylthiourea (10-20 mM) and N-(2-mercaptopropionyl)-glycine (20 mM). The hydroxyl radical scavenger, dimethyl sulfoxide (200-400 mM), also reduced injury. Other scavengers that probably remained extracellular, superoxide dismutase and mannitol, were ineffective. Thus, with exposure of cardiac myocytes to H2O2, cytotoxicity requires reactions catalyzed by intracellular iron.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Corazón
/
Peróxido de Hidrógeno
/
Hierro
Límite:
Animals
Idioma:
En
Revista:
Am J Physiol
Año:
1994
Tipo del documento:
Article
Pais de publicación:
Estados Unidos