Biochim Biophys Acta. 2006 Feb;1762(2):223-31. Epub 2005 Oct 21.

Mitochondrial dysfunction in cardiac ischemia-reperfusion injury: ROS from complex I, without inhibition.

Tompkins AJ, Burwell LS, Digerness SB, Zaragoza C, Holman WL, Brookes PS.

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Departments of Anesthesiology, and Biochemistry & Molecular Biology, Box 604, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester NY 14642, USA.

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.

PMID:: 16278076; [PubMed - indexed for MEDLINE]

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