Wijermars 2016 Am J Transplant
Wijermars LG, Schaapherder AF, Kostidis S, Wรผst RC, Lindeman JH (2016) Succinate accumulation and ischemia reperfusion injury: of mice but not men - A study in renal ischemia reperfusion. Am J Transplant 16:2741-6. |
Wijermars LG, Schaapherder AF, Kostidis S, Wuest Rob CI, Lindeman Jan HN (2016) Am J Transplant
Abstract: A recent seminal paper implicated ischemia-related succinate accumulation followed by succinate driven-reactive oxygen species formation as key driver of ischemia reperfusion injury. Although the data show that the mechanism is universal for all organs tested (kidney, liver, heart and brain), a remaining question is to what extend these observations for mouse translate to man. We here show that succinate accumulation is not a universal event during ischemia, and does not occur during renal graft procurement, in fact tissue succinate content progressively decreases with advancing graft ischemia time (p<0.007). Contrasting responses were also found with respect to mitochondrial susceptibility towards ischemia and reperfusion, with rodent mitochondria robustly resistant towards warm ischemia, but human and pig mitochondria being highly susceptible to warm ischemia (p<0.05). These observations suggest that succinate-driven reactive oxygen formation does not occur in the context of kidney transplantation. In fact absent allantoin release from the reperfused grafts suggests minimal oxidative stress during clinical reperfusion.
This article is protected by copyright. All rights reserved.
โข O2k-Network Lab: NL Amsterdam Wuest RC, NL Leiden Lindeman JHN
Labels: MiParea: Respiration, Comparative MiP;environmental MiP, mt-Medicine
Stress:Ischemia-reperfusion, Oxidative stress;RONS Organism: Human, Pig, Mouse, Rat Tissue;cell: Kidney Preparation: Permeabilized tissue
Coupling state: LEAK, OXPHOS, ET
Pathway: N, S, NS, ROX
HRR: Oxygraph-2k
2016-07