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Difference between revisions of "Gnaiger 2000 Life in the Cold"

From Bioblast
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|tissues=Heart
|tissues=Heart
|preparations=Permeabilized tissue, Isolated mitochondria
|preparations=Permeabilized tissue, Isolated mitochondria
|injuries=Ischemia-reperfusion;preservation
|injuries=Ischemia-reperfusion
|topics=Cyt c, Ion;substrate transport, Substrate, Temperature
|topics=Cyt c, Ion;substrate transport, Substrate, Temperature
|couplingstates=OXPHOS
|couplingstates=OXPHOS

Revision as of 07:34, 16 June 2015

Publications in the MiPMap
O2k-Protocols contents

Gnaiger E, Kuznetsov AV, Schneeberger S, Seiler R, Brandacher G, Steurer W, Margreiter R (2000) Mitochondria in the cold. In: Life in the Cold (Heldmaier G, Klingenspor M, eds) Springer, Heidelberg, Berlin, New York:431-42.

Β» Bioblast Access

Gnaiger E, Kuznetsov AV, Schneeberger S, Seiler R, Brandacher G, Steurer W, Margreiter R (2000) Springer

Abstract: Development of hibernation strategies for cold preservation of human organs represents a far-reaching goal in transplantation surgery. Short cold storage times of <6 h tolerated by the human heart remain a major clinical problem. Mitochondrial cold storage-reperfusion injury is becoming recognized as a limiting factor in preservation of organs from non-hibernating mammals. Damaged mitochondria lead to cellular injury by reduction of ATP supply, oxidative stress, disturbance of ion balance, cytochrome c release and induction of apoptosis and necrosis. Profiles of mitochondrial injuries differed after (1) cold preservation of isolated rat heart mitochondria, (2) cold preservation of the rat heart, and (3) after transplantation and rewarming/reperfusion. Importantly, a specific defect of complex I of the electron transport chain, uncoupling of oxidative phosphorylation and the pronounced release of cytochrome c from mitochondria were absent after cold storage but developed during reperfusion, in proportion to the loss of heart function. Cold preservation of isolated heart mitochondria could be significantly prolonged by a mitochondrial preservation solution containing antioxidants, mitochondrial substrates, ATP, histidine, and oncotic agents. Successful cold storage of heart mitochondria demonstrates a large scope for improvement of heart preservation solutions. In this context, comparison of intracellular conditions and cold ischemia-reperfusion injury in hibernating and non-hibernating mammals may provide a rationale for improvement of clinical organ hibernation strategies. β€’ Keywords: MiR05, MiR06

β€’ O2k-Network Lab: AT Innsbruck Gnaiger E, AT Innsbruck OROBOROS


Labels: MiParea: Respiration, Instruments;methods, mt-Medicine, Pharmacology;toxicology 

Stress:Ischemia-reperfusion  Organism: Rat  Tissue;cell: Heart  Preparation: Permeabilized tissue, Isolated mitochondria 

Regulation: Cyt c, Ion;substrate transport, Substrate, Temperature  Coupling state: OXPHOS 

HRR: Oxygraph-2k, Protocol"Protocol" is not in the list (Oxygraph-2k, TIP2k, O2k-Fluorometer, pH, NO, TPP, Ca, O2k-Spectrophotometer, O2k-Manual, O2k-Protocol, ...) of allowed values for the "Instrument and method" property. 


  • Referred to in Gnaiger_2014_MitoPathways, Chapter 1.
  • This publication contains the original description of the mitochondrial respiration medium MiR05 (see MiR06).