Open AccessH2O2-mediated oxidative stress versus cold ischemia-reperfusion: mitochondrial respiratory defects in cultured human endothelial cells
Author(s) -
Sylvia Stadlmann,
Gunde Rieger,
Albert Amberger,
Andrey V. Kuznetsov,
Raimund Margreiter,
Erich Gnaiger
Publication year - 2002
Publication title -
transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.45
H-Index - 204
eISSN - 1534-6080
pISSN - 0041-1337
DOI - 10.1097/00007890-200212270-00029
Subject(s) - oxidative stress , ischemia , mitochondrion , respiration , respirometry , endothelium , oxidative phosphorylation , reperfusion injury , reactive oxygen species , cellular respiration , chemistry , biology , andrology , endocrinology , medicine , biochemistry , anatomy
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.