Difference between revisions of "Stadlmann 2002 Transplantation"
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|abstract=Oxidative stress to vascular endothelium plays an important role in cold ischemia-reperfusion (CIR) injury. We compared mitochondrial and plasma membrane integrity in human endothelial cells after 20-min exposure to 500 µM H<sub>2</sub>O<sub>2</sub> or 8-hr cold ischemia and simulated reperfusion. In both groups, plasma membrane integrity was maintained but respiration was significantly decreased, as measured by high-resolution respirometry. Uncoupling was more pronounced after H<sub>2</sub>O<sub>2</sub> exposure compared with CIR. After H<sub>2</sub>O<sub>2</sub> exposure, complex I respiration was significantly reduced, whereas CIR resulted additionally in a significant inhibition of complex II and IV respiration. Our results point to a partial overlap of the patterns of mitochondrial defects after H2O2-mediated and CIR injury. In this respect, H<sub>2</sub>O<sub>2</sub> exposure proved to be a useful model to study the mechanisms of CIR injury to human endothelial cells, whereas the full pattern of CIR injury could not be induced by a pulse of hydrogen peroxide exposure. | |abstract=Oxidative stress to vascular endothelium plays an important role in cold ischemia-reperfusion (CIR) injury. We compared mitochondrial and plasma membrane integrity in human endothelial cells after 20-min exposure to 500 µM H<sub>2</sub>O<sub>2</sub> or 8-hr cold ischemia and simulated reperfusion. In both groups, plasma membrane integrity was maintained but respiration was significantly decreased, as measured by high-resolution respirometry. Uncoupling was more pronounced after H<sub>2</sub>O<sub>2</sub> exposure compared with CIR. After H<sub>2</sub>O<sub>2</sub> exposure, complex I respiration was significantly reduced, whereas CIR resulted additionally in a significant inhibition of complex II and IV respiration. Our results point to a partial overlap of the patterns of mitochondrial defects after H2O2-mediated and CIR injury. In this respect, H<sub>2</sub>O<sub>2</sub> exposure proved to be a useful model to study the mechanisms of CIR injury to human endothelial cells, whereas the full pattern of CIR injury could not be induced by a pulse of hydrogen peroxide exposure. | ||
|keywords=Latent mitochondrial dysfunction | |keywords=Latent mitochondrial dysfunction | ||
|mipnetlab= | |mipnetlab=AT Innsbruck Gnaiger E, AT Innsbruck OROBOROS | ||
|discipline=Mitochondrial Physiology, Biomedicine | |discipline=Mitochondrial Physiology, Biomedicine | ||
}} | }} | ||
Revision as of 12:27, 20 March 2015
| Stadlmann S, Rieger G, Amberger A, Kuznetsov AV, Margreiter R, Gnaiger E (2002) H2O2-mediated oxidative stress versus cold ischemia-reperfusion: mitochondrial respiratory defects in cultured human endothelial cells. Transplantation 74:1800-3. |
Stadlmann S, Rieger G, Amberger A, Kuznetsov AV, Margreiter R, Gnaiger E (2002) Transplantation
Abstract: Oxidative stress to vascular endothelium plays an important role in cold ischemia-reperfusion (CIR) injury. We compared mitochondrial and plasma membrane integrity in human endothelial cells after 20-min exposure to 500 µM H2O2 or 8-hr cold ischemia and simulated reperfusion. In both groups, plasma membrane integrity was maintained but respiration was significantly decreased, as measured by high-resolution respirometry. Uncoupling was more pronounced after H2O2 exposure compared with CIR. After H2O2 exposure, complex I respiration was significantly reduced, whereas CIR resulted additionally in a significant inhibition of complex II and IV respiration. Our results point to a partial overlap of the patterns of mitochondrial defects after H2O2-mediated and CIR injury. In this respect, H2O2 exposure proved to be a useful model to study the mechanisms of CIR injury to human endothelial cells, whereas the full pattern of CIR injury could not be induced by a pulse of hydrogen peroxide exposure. • Keywords: Latent mitochondrial dysfunction
• O2k-Network Lab: AT Innsbruck Gnaiger E, AT Innsbruck OROBOROS
Labels: MiParea: Respiration, mt-Medicine
Pathology: Cardiovascular
Stress:Ischemia-reperfusion;preservation"Ischemia-reperfusion;preservation" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property., Oxidative stress;RONS
Organism: Human
Tissue;cell: Endothelial;epithelial;mesothelial cell
Preparation: Intact cells, Permeabilized cells
Regulation: Coupling efficiency;uncoupling, Substrate;glucose;TCA cycle"Substrate;glucose;TCA cycle" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property. Coupling state: LEAK, ROUTINE, OXPHOS
HRR: Oxygraph-2k
Latent mitochondrial dysfunction
