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Difference between revisions of "Stadlmann 2002 Transplantation"

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{{Publication
{{Publication
|title=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.
|title=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.
|authors=Stadlmann S, Rieger G, Amberger A, Kuznetsov AV, Margreiter R, Gnaiger E
|info=[http://www.ncbi.nlm.nih.gov/pubmed/12499903 PMID: 12499903]
|authors=Stadlmann S, Rieger G, Amberger A, Kuznetsov AV, Margreiter R, Gnaiger Erich
|year=2002
|year=2002
|journal=Transplantation
|journal=Transplantation
|mipnetlab=AT_Innsbruck_GnaigerE
|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 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>Β  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 Β΅M 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>Β  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.
|info=[http://www.ncbi.nlm.nih.gov/pubmed/12499903 PMID: 12499903]
|keywords=Latent mitochondrial dysfunction
|mipnetlab=AT Innsbruck Gnaiger E, AT Innsbruck Oroboros
}}
}}
== Cited by ==
::* 8 articles in PubMed (2021-12-27) https://pubmed.ncbi.nlm.nih.gov/12499903/
{{Template:Cited by Gnaiger 2020 BEC MitoPathways}}
{{Labeling
{{Labeling
|area=Respiration, mt-Medicine
|organism=Human
|tissues=Endothelial;epithelial;mesothelial cell
|preparations=Intact cells, Permeabilized cells
|injuries=Ischemia-reperfusion, Oxidative stress;RONS
|diseases=Cardiovascular
|topics=Coupling efficiency;uncoupling, Substrate
|couplingstates=LEAK, ROUTINE, OXPHOS
|pathways=N, S, CIV, ROX
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|discipline=Mitochondrial Physiology, Biomedicine
|additional=Latent mitochondrial dysfunction, BEC 2020.2, MitoFit 2021 PLT
|organism=Human
|tissues=Endothelial; Epithelial; Mesothelial Cell
|preparations=Intact Cell; Cultured; Primary, Permeabilized Cell or Tissue; Homogenate
|injuries=Ischemia-Reperfusion; Preservation, RONS; Oxidative Stress
|topics=Respiration; OXPHOS; ETS Capacity, Coupling; Membrane Potential, Substrate; Glucose; TCA Cycle
}}
}}

Latest revision as of 13:10, 27 December 2021

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 74:1800-3.

Β» PMID: 12499903

Stadlmann S, Rieger G, Amberger A, Kuznetsov AV, Margreiter R, Gnaiger Erich (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 Oroboros


Cited by

Gnaiger 2020 BEC MitoPathways
Gnaiger E (2020) Mitochondrial pathways and respiratory control. An introduction to OXPHOS analysis. 5th ed. Bioenerg Commun 2020.2. https://doi.org/10.26124/bec:2020-0002



Labels: MiParea: Respiration, mt-Medicine  Pathology: Cardiovascular  Stress:Ischemia-reperfusion, Oxidative stress;RONS  Organism: Human  Tissue;cell: Endothelial;epithelial;mesothelial cell  Preparation: Intact cells, Permeabilized cells 

Regulation: Coupling efficiency;uncoupling, Substrate  Coupling state: LEAK, ROUTINE, OXPHOS  Pathway: N, S, CIV, ROX  HRR: Oxygraph-2k 

Latent mitochondrial dysfunction, BEC 2020.2, MitoFit 2021 PLT