Stadlmann 2002 Transplantation
|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.|
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
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