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Difference between revisions of "Krivakova 2007 Physiol Res"

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{{Publication
{{Publication
|title=Krivakova P, Labajova A, Cervinkova Z, Drahota Z (2007) Inhibitory effect of t-butyl hydroperoxide on mitochondrial oxidative phosphorylation in isolated rat hepatocytes. Physiol Res. 56: 137-140.
|title=Krivakova P, Labajova A, Cervinkova Z, Drahota Z (2007) Inhibitory effect of t-butyl hydroperoxide on mitochondrial oxidative phosphorylation in isolated rat hepatocytes. Physiol Res 56: 137-140.
|info=[http://www.ncbi.nlm.nih.gov/pubmed/17381246 PMID: 17381246]
|info=[http://www.ncbi.nlm.nih.gov/pubmed/17381246 PMID: 17381246]
|authors=Krivakova P, Labajova A, Cervinkova Z, Drahota Z
|authors=Krivakova P, Labajova A, Cervinkova Z, Drahota Z

Revision as of 16:41, 11 December 2011

Publications in the MiPMap
Krivakova P, Labajova A, Cervinkova Z, Drahota Z (2007) Inhibitory effect of t-butyl hydroperoxide on mitochondrial oxidative phosphorylation in isolated rat hepatocytes. Physiol Res 56: 137-140.

Β» PMID: 17381246

Krivakova P, Labajova A, Cervinkova Z, Drahota Z (2007) Physiol. Res.

Abstract: Using high-resolution oxygraphy, we tested the changes of various parameters characterizing the mitochondrial energy provision system that were induced by peroxidative damage. In the presence of succinate as respiratory substrate, 3 mM t-butyl hydroperoxide increased respiration in the absence of ADP, which indicated partial uncoupling of oxidative phosphorylation. Low activity of coupled respiration was still maintained as indicated by the ADP-activated and oligomycin-inhibited respiration. However, during the incubation the phosphorylative capacity decreased as indicated by the continuous decrease of the mitochondrial membrane potential. Under these experimental conditions the maximum capacity of the succinate oxidase system was inhibited by 50 % in comparison with values obtained in the absence of t-butyl hydroperoxide. Our data thus indicate that the oxygraphic evaluation of mitochondrial function represents a useful tool for evaluation of changes participating in peroxidative damage of cell energy metabolism. β€’ Keywords: Hepatocytes, Oxidative phosphorylation, t-Butyl hydroperoxide

β€’ O2k-Network Lab: CZ_Hradec Kralove_Cervinkova Z


Labels:

Stress:RONS; Oxidative Stress"RONS; Oxidative Stress" 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: Hepatocyte; Liver"Hepatocyte; Liver" 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.  Preparation: Isolated Mitochondria"Isolated Mitochondria" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property. 



HRR: Oxygraph-2k