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

作者：Tompkins AJ; Burwell LS; Digerness SB; Zaragoza C; Holman WL; Brookes PS^*

来源：Biochimica et Biophysica Acta-Molecular Basis of Disease, 2006, 1762(2): 223-231.

DOI：10.1016/j.bbadis.2005.10.001

• ROS
• ischemia
• mitochondria
• complex 1
• nitric oxide

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 la sub-complex of Cxl. These thiol modifications were accompanied by enhanced ROS generation from Cxl, but not complex III. Implications for the patholog of cardiac I-R injury are discussed.

• 出版日期2006-2