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Difference between revisions of "Stadlmann 2002 Transplantation"

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{{Labeling
{{Labeling
|instruments=Oxygraph-2k
|injuries=Ischemia-Reperfusion; Preservation, RONS; Oxidative Stress
|organism=Human
|organism=Human
|tissues=Endothelial; Epithelial; Mesothelial Cell
|tissues=Endothelial; Epithelial; Mesothelial Cell
|preparations=Intact Cell; Cultured; Primary, Permeabilized cells
|preparations=Intact cells, Permeabilized cells
|injuries=Ischemia-Reperfusion; Preservation, RONS; Oxidative Stress
|topics=Substrate; Glucose; TCA Cycle
|couplingstates=OXPHOS
|couplingstates=OXPHOS
|topics=Substrate; Glucose; TCA Cycle
|instruments=Oxygraph-2k
|additional=Latent mitochondrial dysfunction, Environmental Physiology; Toxicology
|additional=Latent mitochondrial dysfunction, Environmental Physiology; Toxicology
|discipline=Mitochondrial Physiology, Biomedicine
|discipline=Mitochondrial Physiology, Biomedicine
}}
}}

Revision as of 08:16, 8 August 2013

Publications in the MiPMap
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: 1800-1803.

Β» PMID: 12499903

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 Β΅M 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. β€’ Keywords: Latent mitochondrial dysfunction

β€’ O2k-Network Lab: AT_Innsbruck_Gnaiger E, AT Innsbruck MitoCom


Labels:

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., RONS; Oxidative Stress"RONS; Oxidative Stress" 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.  Organism: Human  Tissue;cell: Endothelial; Epithelial; Mesothelial Cell"Endothelial; Epithelial; Mesothelial Cell" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property.  Preparation: Intact cells, Permeabilized cells 

Regulation: 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: OXPHOS 

HRR: Oxygraph-2k 

Latent mitochondrial dysfunction, Environmental Physiology; Toxicology