1 40 1 Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1007/s00395-017-0626-1" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s00395-017-0626-1</a> Pages 36–36 Issue 4 Volume 112 Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Impairment of pH gradient and membrane potential mediates redox dysfunction in the mitochondria of the post-ischemic heart. Publisher An entity responsible for making the resource available Basic research in cardiology Date A point or period of time associated with an event in the lifecycle of the resource 2017 2017-07 Subject The topic of the resource *Energy Metabolism; *Membrane potential; *Membrane Potential; *Mitochondria; *Myocardial ischemia and reperfusion; *Oxidative Stress; *pH gradient; *Redox dysfunction; Aconitate Hydratase/metabolism; Animal; Animals; Cell Line; Disease Models; Electron Transport Chain Complex Proteins/metabolism; Heart/*metabolism/pathology; Hydrogen Peroxide/metabolism; Hydrogen-Ion Concentration; Ionophores/pharmacology; Male; Mitochondria; Mitochondrial; Myocardial Infarction/*metabolism/pathology; Myocardium/*metabolism/pathology; Oxidation-Reduction; Potassium/metabolism; Rats; Sprague-Dawley; Superoxides/metabolism Creator An entity primarily responsible for making the resource Kang Patrick T; Chen Chwen-Lih; Lin Paul; Chilian William M; Chen Yeong-Renn Description An account of the resource The mitochondrial electrochemical gradient (Deltap), which comprises the pH gradient (DeltapH) and the membrane potential (DeltaPsi), is crucial in controlling energy transduction. During myocardial ischemia and reperfusion (IR), mitochondrial dysfunction mediates superoxide ((.)O2(-)) and H2O2 overproduction leading to oxidative injury. However, the role of DeltapH and DeltaPsi in post-ischemic injury is not fully established. Here we studied mitochondria from the risk region of rat hearts subjected to 30 min of coronary ligation and 24 h of reperfusion in vivo. In the presence of glutamate, malate and ADP, normal mitochondria (mitochondria of non-ischemic region, NR) exhibited a heightened state 3 oxygen consumption rate (OCR) and reduced (.)O2(-) and H2O2 production when compared to state 2 conditions. Oligomycin (increases DeltapH by inhibiting ATP synthase) increased (.)O2(-) and H2O2 production in normal mitochondria, but not significantly in the mitochondria of the risk region (IR mitochondria or post-ischemic mitochondria), indicating that normal mitochondrial (.)O2(-) and H2O2 generation is dependent on DeltapH and that IR impaired the DeltapH of normal mitochondria. Conversely, nigericin (dissipates DeltapH) dramatically reduced (.)O2(-) and H2O2 generation by normal mitochondria under state 4 conditions, and this nigericin quenching effect was less pronounced in IR mitochondria. Nigericin also increased mitochondrial OCR, and predisposed normal mitochondria to a more oxidized redox status assessed by increased oxidation of cyclic hydroxylamine, CM-H. IR mitochondria, although more oxidized than normal mitochondria, were not responsive to nigericin-induced CM-H oxidation, which is consistent with the result that IR induced DeltapH impairment in normal mitochondria. Valinomycin, a K(+) ionophore used to dissipate DeltaPsi, drastically diminished (.)O2(-) and H2O2 generation by normal mitochondria, but less pronounced effect on IR mitochondria under state 4 conditions, indicating that DeltaPsi also contributed to (.)O2(-) generation by normal mitochondria and that IR mediated DeltaPsi impairment. However, there was no significant difference in valinomycin-induced CM-H oxidation between normal and IR mitochondria. In conclusion, under normal conditions the proton backpressure imposed by DeltapH restricts electron flow, controls a limited amount of (.)O2(-) generation, and results in a more reduced myocardium; however, IR causes DeltapH impairment and prompts a more oxidized myocardium. Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1007/s00395-017-0626-1" target="_blank" rel="noreferrer noopener">10.1007/s00395-017-0626-1</a> Rights Information about rights held in and over the resource Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). *Energy Metabolism *Membrane potential *Mitochondria *Myocardial ischemia and reperfusion *Oxidative Stress *pH gradient *Redox dysfunction 2017 Aconitate Hydratase/metabolism Animal Animals Basic research in cardiology Cell Line Chen Chwen-Lih Chen Yeong-Renn Chilian William M Department of Family & Community Medicine Department of Integrative Medical Sciences Disease Models Electron Transport Chain Complex Proteins/metabolism Heart/*metabolism/pathology Hydrogen Peroxide/metabolism Hydrogen-Ion Concentration Ionophores/pharmacology Kang Patrick T Lin Paul Male Mitochondria Mitochondrial Myocardial Infarction/*metabolism/pathology Myocardium/*metabolism/pathology NEOMED College of Medicine Oxidation-Reduction Potassium/metabolism Rats Sprague-Dawley Superoxides/metabolism