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.

» PMDI: 10083442

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 Oroboros

Labels:

Stress:Ischemia-reperfusion, Oxidative stress;RONS  Organism: Human  Tissue;cell: Endothelial;epithelial;mesothelial cell  Preparation: Intact cells 

Coupling state: OXPHOS 

HRR: Oxygraph-2k