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Difference between revisions of "Stadlmann 2002 Transplantation"

From Bioblast
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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 ยตM 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>ย  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 ยตM 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>ย  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=AT_Innsbruck_Gnaiger E, AT Innsbruck MitoCom
|mipnetlab=AT_Innsbruck_Gnaiger E, AT Innsbruck OROBOROS,
|discipline=Mitochondrial Physiology, Biomedicine
|discipline=Mitochondrial Physiology, Biomedicine
}}
}}
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|substratestates=CI, CII, CIV, ROX
|substratestates=CI, CII, CIV, ROX
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|additional=Latent mitochondrial dysfunction, Environmental Physiology; Toxicology
|additional=Latent mitochondrial dysfunction
|discipline=Mitochondrial Physiology, Biomedicine
|discipline=Mitochondrial Physiology, Biomedicine
}}
}}

Revision as of 19:16, 15 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.

ยป 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 ยตM 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. โ€ข Keywords: Latent mitochondrial dysfunction

โ€ข 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., 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: 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