Gnaiger 2000 Life in the Cold
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 |
Β» - Springer link
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. β’ Keywords: MiR05, MiR06
β’ O2k-Network Lab: AT Innsbruck Oroboros
MiR05-Kit
- * This publication contains the original description of the mitochondrial respiration medium MiR05-Kit.
Cited by
- Baglivo E, Cardoso LHD, Cecatto C, Gnaiger E (2024) Stability of mitochondrial respiration medium used in high-resolution respirometry with living and permeabilized cells. Bioenerg Commun 2024.8. https://doi.org/10.26124/bec.2024-0008
- Gnaiger E (2020) Mitochondrial pathways and respiratory control. An introduction to OXPHOS analysis. 5th ed. Bioenerg Commun 2020.2. https://doi.org/10.26124/bec:2020-0002
- Cardoso et al (2021) Magnesium Green for fluorometric measurement of ATP production does not interfere with mitochondrial respiration. Bioenerg Commun 2021.1. doi:10.26124/bec:2021-0001
- KomlΓ³di T, Cardoso LHD, Doerrier C, Moore AL, Rich PR, Gnaiger E (2021) Coupling and pathway control of coenzyme Q redox state and respiration in isolated mitochondria. Bioenerg Commun 2021.3. https://doi.org/10.26124/bec:2021-0003
- KomlΓ³di T, Sobotka O, Gnaiger E (2021) Facts and artefacts on the oxygen dependence of hydrogen peroxide production using Amplex UltraRed. Bioenerg Commun 2021.4. https://doi:10.26124/BEC:2021-0004
- 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. - Β»Bioblast linkΒ«
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
MiR05, BEC 2020.2, MitoFit 2021 MgG, MitoFit 2021 CoQ, MitoFit 2022 NADH, MitoFit 2021 AmR-O2, MitoFit2022QC, Baglivo 2024 BEC