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| {{Publication
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| |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.
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| |info=[http://www.ncbi.nlm.nih.gov/pubmed/12499903 PMID: 12499903]
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| |authors=Stadlmann S, Rieger G, Amberger A, Kuznetsov AV, Margreiter R, Gnaiger E
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| |year=2002
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| |journal=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.
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| |keywords=Latent mitochondrial dysfunction
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| |mipnetlab=AT Innsbruck Gnaiger E, AT Innsbruck Oroboros
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| |discipline=Mitochondrial Physiology, Biomedicine
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| }}
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| {{Labeling
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| |area=Respiration, mt-Medicine
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| |organism=Human
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| |tissues=Endothelial;epithelial;mesothelial cell
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| |preparations=Intact cells, Permeabilized cells
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| |injuries=Ischemia-reperfusion, Oxidative stress;RONS
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| |diseases=Cardiovascular
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| |topics=Coupling efficiency;uncoupling, Substrate
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| |couplingstates=LEAK, ROUTINE, OXPHOS
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| |pathways=N, S, CIV, ROX
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| |instruments=Oxygraph-2k
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| |additional=Latent mitochondrial dysfunction
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| |discipline=Mitochondrial Physiology, Biomedicine
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| }}
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