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Mechanisms of reoxygenation injury in myocardial infarction: implications of a myoglobin redox cycle.
Galaris, D; Eddy, L; Arduini, A; Cadenas, E; Hochstein, P.
Afiliación
  • Galaris D; Institute for Toxicology, University of Southern California, Los Angeles 90033.
Biochem Biophys Res Commun ; 160(3): 1162-8, 1989 May 15.
Article en En | MEDLINE | ID: mdl-2730642
ABSTRACT
The addition of ascorbate to ischemic rat hearts prevents the myocardial damage associated with reoxygenation. H2O2 oxidizes myoglobin (Mb+2) to higher oxidation states (Mb+4 and Mb+5) which are rapidly reduced by ascorbate. It is proposed that the operation of a myoglobin redox cycle, in which H2O2 causes the two-electron oxidation of myoglobin, is a critical determinant of reperfusion injury. Conversely, the reduction of myoglobin, in one-electron steps, may represent an essential protective mechanism against such injury in the heart.
Asunto(s)
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Daño por Reperfusión Miocárdica / Infarto del Miocardio / Mioglobina Tipo de estudio: Etiology_studies Límite: Animals Idioma: En Revista: Biochem Biophys Res Commun Año: 1989 Tipo del documento: Article
Buscar en Google
Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Daño por Reperfusión Miocárdica / Infarto del Miocardio / Mioglobina Tipo de estudio: Etiology_studies Límite: Animals Idioma: En Revista: Biochem Biophys Res Commun Año: 1989 Tipo del documento: Article