Difference between revisions of "Stadlmann 2002 Transplantation"
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{{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 74:1800-3. | |||
|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 | |||
|journal=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 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 | |||
|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 | |||
|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 | |||
|additional=Latent mitochondrial dysfunction, BEC 2020.2, MitoFit 2021 PLT | |||
}} | |||
Latest revision as of 14:10, 27 December 2021
| 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 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 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
Cited by
- 8 articles in PubMed (2021-12-27) https://pubmed.ncbi.nlm.nih.gov/12499903/
- 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
