Labajova 2006 Gen Physiol Biophys: Difference between revisions
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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 | |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. | ||
|authors=Labajova | |info=[http://www.ncbi.nlm.nih.gov/pubmed/17197730 PMID: 17197730 Open Access] | ||
|authors=Labajova Anna, Kofranek J, Stankova Pavla, Cervinkova Zuzana, Drahota Zdenek | |||
|year=2006 | |year=2006 | ||
|journal=Gen | |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 | ||
|discipline=Mitochondrial Physiology | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
|organism=Rat | |organism=Rat | ||
|tissues= | |tissues=Liver | ||
| | |preparations=Permeabilized cells | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|discipline=Mitochondrial Physiology | |||
}} | }} |
Latest revision as of 11:14, 18 March 2020
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. |
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
Labels:
Organism: Rat
Tissue;cell: Liver
Preparation: Permeabilized cells
HRR: Oxygraph-2k