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

Departments of Anesthesiology, and Biochemistry & Molecular Biology, Box 604, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester NY 14642, USA.
Biochimica et Biophysica Acta (Impact Factor: 4.66). 03/2006; 1762(2):223-31. DOI: 10.1016/j.bbadis.2005.10.001
Source: PubMed


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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Available from: Lindsay Burwell, Mar 03, 2015
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