Mitochondrial dysfunction in cardiac ischemia-reperfusion injury: ROS from complex I, without inhibition.
Biochim Biophys Acta
; 1762(2): 223-31, 2006 Feb.
Article
en En
| MEDLINE
| ID: mdl-16278076
ABSTRACT
A key pathologic event in cardiac ischemia reperfusion (I-R) injury is mitochondrial energetic dysfunction, and several studies have attributed this to complex I (CxI) inhibition. In isolated perfused rat hearts, following I-R, we found that CxI-linked respiration was inhibited, but isolated CxI enzymatic activity was not. Using the mitochondrial thiol probe iodobutyl-triphenylphosphonium in conjunction with proteomic tools, thiol modifications were identified in several subunits of the matrix-facing 1alpha sub-complex of CxI. These thiol modifications were accompanied by enhanced ROS generation from CxI, but not complex III. Implications for the pathology of cardiac I-R injury are discussed.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Daño por Reperfusión Miocárdica
/
Especies Reactivas de Oxígeno
/
Isquemia Miocárdica
/
Complejo I de Transporte de Electrón
/
Mitocondrias Cardíacas
Límite:
Animals
Idioma:
En
Revista:
Biochim Biophys Acta
Año:
2006
Tipo del documento:
Article
País de afiliación:
Estados Unidos