Difference between revisions of "Pasdois 2006 J Bioenerg Biomembr"
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|year=2006 | |year=2006 | ||
|journal=J. Bioenerg. Biomembr. | |journal=J. Bioenerg. Biomembr. | ||
|abstract=It has been proposed that activation of the mitochondrial ATP-sensitive potassium channel (mitoKATP) is part of signaling pathways triggering the cardioprotection afforded by ischemic preconditioning of the heart. This work was to analyze the mitochondrial function profile of Langendorff-perfused rat hearts during the different phases of various ischemia-reperfusion protocols. Specifically, skinned fibers of ischemic preconditioned hearts exhibit a decline in the succinate-supported respiration and complex II activity during ischemia, followed by a recovery during reperfusion. Meanwhile, the apparent affinity of respiration for ADP (which reflects the matrix volume expansion) is increased during preconditioning stimulus and, to a larger extent, during prolonged ischemia. This evolution pattern is mimicked by diazoxide and abolished by 5-hydroxydecanoate. It is concluded that opening the mitoKATP channel mediates the preservation of mitochondrial structure-function via a mitochondrial matrix shrinkage and a reversible inactivation of complex II during prolonged ischemic insult. | |abstract=It has been proposed that activation of the mitochondrial ATP-sensitive potassium channel (mitoKATP) is part of signaling pathways triggering the cardioprotection afforded by ischemic preconditioning of the heart. This work was to analyze the mitochondrial function profile of Langendorff-perfused rat hearts during the different phases of various ischemia-reperfusion protocols. Specifically, skinned fibers of ischemic preconditioned hearts exhibit a decline in the succinate-supported respiration and complex II activity during ischemia, followed by a recovery during reperfusion. Meanwhile, the apparent affinity of respiration for ADP (which reflects the matrix volume expansion) is increased during preconditioning stimulus and, to a larger extent, during prolonged ischemia. This evolution pattern is mimicked by diazoxide and abolished by 5-hydroxydecanoate. It is concluded that opening the mitoKATP channel mediates the preservation of mitochondrial structure-function via a mitochondrial matrix shrinkage and a reversible inactivation of complex II during prolonged ischemic insult. | ||
|keywords=MitokATP, Diazoxide, Ischemic preconditioning, Succinate dehydrogenase, Complex II | |keywords=MitokATP, Diazoxide, Ischemic preconditioning, Succinate dehydrogenase, Complex II | ||
|mipnetlab=FR_Pessak_Beauvoit B | |||
|discipline=Biomedicine | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
| | |instruments=Oxygraph-2k | ||
|injuries=Ischemia-Reperfusion; Preservation | |injuries=Ischemia-Reperfusion; Preservation | ||
|organism=Rat | |organism=Rat | ||
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|enzymes=Complex II; Succinate Dehydrogenase, Inner mtMembrane Transporter | |enzymes=Complex II; Succinate Dehydrogenase, Inner mtMembrane Transporter | ||
|topics=Respiration; OXPHOS; ETS Capacity | |topics=Respiration; OXPHOS; ETS Capacity | ||
| | |discipline=Biomedicine | ||
}} | }} | ||
Revision as of 09:48, 12 August 2011
| Pasdois P, Beauvoit B, Tariosse L, Vinassa B, Bonoron-Adèle S, Santos PD (2006) MitoK(ATP)-dependent changes in mitochondrial volume and in complex II activity during ischemic and pharmacological preconditioning of Langendorff-perfused rat heart. J. Bioenerg. Biomembr. 38: 101-112. |
Pasdois P, Beauvoit B, Tariosse L, Vinassa B, Bonoron-Adele S, Santos PD (2006) J. Bioenerg. Biomembr.
Abstract: It has been proposed that activation of the mitochondrial ATP-sensitive potassium channel (mitoKATP) is part of signaling pathways triggering the cardioprotection afforded by ischemic preconditioning of the heart. This work was to analyze the mitochondrial function profile of Langendorff-perfused rat hearts during the different phases of various ischemia-reperfusion protocols. Specifically, skinned fibers of ischemic preconditioned hearts exhibit a decline in the succinate-supported respiration and complex II activity during ischemia, followed by a recovery during reperfusion. Meanwhile, the apparent affinity of respiration for ADP (which reflects the matrix volume expansion) is increased during preconditioning stimulus and, to a larger extent, during prolonged ischemia. This evolution pattern is mimicked by diazoxide and abolished by 5-hydroxydecanoate. It is concluded that opening the mitoKATP channel mediates the preservation of mitochondrial structure-function via a mitochondrial matrix shrinkage and a reversible inactivation of complex II during prolonged ischemic insult. • Keywords: MitokATP, Diazoxide, Ischemic preconditioning, Succinate dehydrogenase, Complex II
• O2k-Network Lab: FR_Pessak_Beauvoit B
Labels:
Stress:Ischemia-Reperfusion; Preservation"Ischemia-Reperfusion; Preservation" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. Organism: Rat Tissue;cell: Cardiac Muscle"Cardiac Muscle" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property.
Enzyme: Complex II; Succinate Dehydrogenase"Complex II; Succinate Dehydrogenase" is not in the list (Adenine nucleotide translocase, Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase, Inner mt-membrane transporter, Marker enzyme, Supercomplex, TCA cycle and matrix dehydrogenases, ...) of allowed values for the "Enzyme" property., Inner mtMembrane Transporter"Inner mtMembrane Transporter" is not in the list (Adenine nucleotide translocase, Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase, Inner mt-membrane transporter, Marker enzyme, Supercomplex, TCA cycle and matrix dehydrogenases, ...) of allowed values for the "Enzyme" property. Regulation: Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS Capacity" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property.
HRR: Oxygraph-2k
