H2O2-mediated oxidative stress versus cold ischemia-reperfusion: mitochondrial respiratory defects in cultured human endothelial cells.
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 microM H2O 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 H2O exposure compared with CIR. After H2O 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 H2O-mediated and CIR injury. In this respect, H2O 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.
Stadlmann
Sylvia
S
Department of Pathology, University of Innsbruck, Innsbruck, Austria.
Rieger
Gunde
G
Amberger
Albert
A
Kuznetsov
Andrey V
AV
Margreiter
Raimund
R
Gnaiger
Erich
E
D002462:Cell Membrane / Q000378:metabolism; D019069:Cell Respiration; D004730:Endothelium, Vascular / Q000166:cytology* / Q000378:metabolism; D006085:Graft Survival / Q000502:physiology; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology; D007036:Hypothermia, Induced; D008175:Lung Neoplasms; D008928:Mitochondria / Q000378:metabolism*; D016877:Oxidants / Q000494:pharmacology; D018384:Oxidative Stress; D015427:Reperfusion Injury / Q000378:metabolism*; D014407:Tumor Cells, Cultured
D016877:Oxidants; D006861:Hydrogen Peroxide