Gnaiger 2000 Life in the Cold

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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, Berlin, Heidelberg:431-42. https://doi.org/10.1007/978-3-662-04162-8_45

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O2k-Protocols contents

Gnaiger Erich, 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.

Keywords: MiR05, MiR06

O2k-Network Lab: AT Innsbruck Gnaiger E, AT Innsbruck Oroboros

MiR05-Kit

* This publication contains the original description of the mitochondrial respiration medium MiR05-Kit.

Cited by

Gnaiger 2020 BEC MitoPathways


Gnaiger E (2020) Mitochondrial pathways and respiratory control. An introduction to OXPHOS analysis. 5th ed. Bioenerg Commun 2020.2:112 pp. doi:10.26124/bec:2020-0002
  • Cardoso et al (2021) Magnesium Green for fluorometric measurement of ATP production does not interfere with mitochondrial respiration. MitoFit Preprints 2021.1. doi:10.26124/mitofit:2021-0001
  • Komlodi et al (2021) Simultaneous measurement of respiration and redox state of the Coenzyme Q pool in mitochondrial preparations. MitoFit Preprints 2021.2. doi:10.26124/mitofit:2021-0002
  • Wollenman LC, Vander Ploeg MR, Miller ML, Zhang Y, Bazil JN (2017) The effect of respiration buffer composition on mitochondrial metabolism and function. PLOS ONE 12:e0187523. - »Bioblast link«


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, O2k-Protocol 

BEC 2020.2, MitoFit 2021 MgG, MitoFit 2021 CoQ, MitoFit 2021 NADH