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Difference between revisions of "Labajova 2006 Gen Physiol Biophys"

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{{Publication
{{Publication
|title=Lábajová A, Kofránek J, Kriváková P, Cervinková Z, Drahota Z (2006) Tetraphenylphosphonium-Selective Electrode as a Tool for Evaluating Mitochondrial Permeability Transition Pore Function in Isolated Rat Hepatocytes. Gen Physiol Biophys 25: 325-331.
|title=Lábajová A, Kofránek J, Kriváková P, Cervinková Z, Drahota Z (2006) Tetraphenylphosphonium-Selective Electrode as a Tool for Evaluating Mitochondrial Permeability Transition Pore Function in Isolated Rat Hepatocytes. Gen Physiol Biophys 25:325-31.
|info=[http://www.ncbi.nlm.nih.gov/pubmed/17197730 PMID: 17197730]
|info=[http://www.ncbi.nlm.nih.gov/pubmed/17197730 PMID: 17197730 Open Access]
|authors=Labajova A, Kofranek J, Krivakova P, Cervinkova Z, Drahota Z
|authors=Labajova Anna, Kofranek J, Stankova Pavla, Cervinkova Zuzana, Drahota Zdenek
|year=2006
|year=2006
|journal=Gen. Physiol. Biophys.
|journal=Gen Physiol Biophys
|abstract=The changes in mitochondrial membrane potential (Δψm) were used as
|abstract=The changes in mitochondrial membrane potential (Δψm) were used as
an indicator for evaluating the mitochondrial permeability transition pore (MPTP) function. We found that ''in sit''u mitochondria in digitonin-permeabilized hepatocytes were coupled and responded to the addition of substrates, inhibitors and uncouplers. Ca<sup>2+</sup>-induced Δψm dissipation was caused by MPTP opening because this process was inhibited by cyclosporin A. MPTP opening was enhanced by the pro-oxidant tert-butyl hydroperoxide.
an indicator for evaluating the mitochondrial permeability transition pore (MPTP) function. We found that ''in sit''u mitochondria in digitonin-permeabilized hepatocytes were coupled and responded to the addition of substrates, inhibitors and uncouplers. Ca<sup>2+</sup>-induced Δψm dissipation was caused by MPTP opening because this process was inhibited by cyclosporin A. MPTP opening was enhanced by the pro-oxidant tert-butyl hydroperoxide.
|keywords=Tetraphenylphosphonium-selective electrode,  Mitochondrial permeability transition pore,  Hepatocytes
|keywords=Tetraphenylphosphonium-selective electrode,  Mitochondrial permeability transition pore,  Hepatocytes
|mipnetlab=CZ_Hradec Kralove_Cervinkova Z
|mipnetlab=CZ Hradec Kralove Cervinkova Z
|discipline=Mitochondrial Physiology
|discipline=Mitochondrial Physiology
}}
}}
{{Labeling
{{Labeling
|organism=Rat
|tissues=Liver
|preparations=Permeabilized cells
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|organism=Rat
|tissues=Hepatocyte; Liver
|preparations=Permeabilized Cells
|topics=Coupling; Membrane Potential
|discipline=Mitochondrial Physiology
|discipline=Mitochondrial Physiology
}}
}}

Latest revision as of 10:14, 18 March 2020

Publications in the MiPMap
Lábajová A, Kofránek J, Kriváková P, Cervinková Z, Drahota Z (2006) Tetraphenylphosphonium-Selective Electrode as a Tool for Evaluating Mitochondrial Permeability Transition Pore Function in Isolated Rat Hepatocytes. Gen Physiol Biophys 25:325-31.

» PMID: 17197730 Open Access

Labajova Anna, Kofranek J, Stankova Pavla, Cervinkova Zuzana, Drahota Zdenek (2006) Gen Physiol Biophys

Abstract: The changes in mitochondrial membrane potential (Δψm) were used as an indicator for evaluating the mitochondrial permeability transition pore (MPTP) function. We found that in situ mitochondria in digitonin-permeabilized hepatocytes were coupled and responded to the addition of substrates, inhibitors and uncouplers. Ca2+-induced Δψm dissipation was caused by MPTP opening because this process was inhibited by cyclosporin A. MPTP opening was enhanced by the pro-oxidant tert-butyl hydroperoxide. Keywords: Tetraphenylphosphonium-selective electrode, Mitochondrial permeability transition pore, Hepatocytes

O2k-Network Lab: CZ Hradec Kralove Cervinkova Z


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Organism: Rat  Tissue;cell: Liver  Preparation: Permeabilized cells 



HRR: Oxygraph-2k