Stadlmann 1999 Transplant Proc
|Stadlmann S, Amberger A, Kuznetsov AV, Rieger G, Hengster P, Margreiter R, Gnaiger E (1999) Does H2O2-mediated oxidative stress reproduce mitochondrial cold preservation/reoxygenation injury in endothelial cells? Transplant Proc 31:993.|
Stadlmann S, Amberger A, Kuznetsov AV, Rieger G, Hengster P, Margreiter R, Gnaiger E (1999) Transplant Proc
Abstract: PRODUCTION of reactive oxygen species is an important mechanism of cold ischemia-reperfusion (CIR) injury.1,2 Among different activated oxygen species, hydrogen peroxide (H2O2) plays a significant role.3,4 However, the precise mechanism of H2O2-mediated cellular injury and the specific cellular sites of H2O2 attack are not well defined. Recent studies suggest that mitochondria are one of the main targets of early reperfusion injury in endothelial cells.5 Thus, the purpose of this study was to evaluate short-term effects of H2O2 on the mitochondrial respiratory chain and mitochondrial membrane potential (MMP) in endothelial cells.
• O2k-Network Lab: AT Innsbruck Gnaiger E
Stress:Ischemia-reperfusion, Oxidative stress;RONS Organism: Human Tissue;cell: Endothelial;epithelial;mesothelial cell Preparation: Intact cells
Coupling state: OXPHOS