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Difference between revisions of "Endlicher 2009 Physiol Res"

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{{Publication
{{Publication
|title=Endlicher R, Kriváková P, Rauchová H, Nůsková H, Cervinková Z, Drahota Z (2009) Peroxidative damage of mitochondrial respiration is substrate-dependent. Physiol. Res.58(5):685-692.
|title=Endlicher R, Kriváková P, Rauchová H, Nůsková H, Cervinková Z, Drahota Z (2009) Peroxidative damage of mitochondrial respiration is substrate-dependent. Physiol. Res. 58: 685-692.
|info=[http://www.ncbi.nlm.nih.gov/pubmed/19093725 PMID:19093725]
|info=[http://www.ncbi.nlm.nih.gov/pubmed/19093725 PMID:19093725]
|authors=Endlicher R, Krivakova P, Rauchova H, Nuskova H, Cervinkova Z, Drahota Z
|authors=Endlicher R, Krivakova P, Rauchova H, Nuskova H, Cervinkova Z, Drahota Z
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|abstract=The concentration-dependence of tert-butyl hydroperoxide (BHP) inhibitory effect on oxygen consumption in isolated rat liver mitochondria was measured in the presence of various respiratory substrates. Strong inhibitory effect at low concentrations of BHP (15-30 microM) was found for oxoglutarate and palmitoyl carnitine oxidation. Pyruvate and glutamate oxidation was inhibited at higher concentrations of BHP (100-200 microM). Succinate oxidation was not affected even at 3.3 mM BHP. Determination of mitochondrial membrane potential has shown that in the presence of NADH-dependent substrates the membrane potential was dissipated by BHP but was completely restored after addition of succinate. Our data thus indicate that beside peroxidative damage of complex I also various mitochondrial NADH-dependent dehydrogenases are inhibited, but to a different extent and with different kinetics. Our data also show that succinate could be an important nutritional substrate protecting hepatocytes during peroxidative damage.
|abstract=The concentration-dependence of tert-butyl hydroperoxide (BHP) inhibitory effect on oxygen consumption in isolated rat liver mitochondria was measured in the presence of various respiratory substrates. Strong inhibitory effect at low concentrations of BHP (15-30 microM) was found for oxoglutarate and palmitoyl carnitine oxidation. Pyruvate and glutamate oxidation was inhibited at higher concentrations of BHP (100-200 microM). Succinate oxidation was not affected even at 3.3 mM BHP. Determination of mitochondrial membrane potential has shown that in the presence of NADH-dependent substrates the membrane potential was dissipated by BHP but was completely restored after addition of succinate. Our data thus indicate that beside peroxidative damage of complex I also various mitochondrial NADH-dependent dehydrogenases are inhibited, but to a different extent and with different kinetics. Our data also show that succinate could be an important nutritional substrate protecting hepatocytes during peroxidative damage.
|keywords=liver mitochondria, mitochondrial enzymes, peroxidative damage, tert-butyl hydroperoxide
|keywords=liver mitochondria, mitochondrial enzymes, peroxidative damage, tert-butyl hydroperoxide
|mipnetlab=CZ_Hradec Kralove_Cervinkova Z,  
|mipnetlab=CZ_Hradec Kralove_Cervinkova Z, CZ Prague Houstek J
}}
}}
{{Labeling
{{Labeling

Revision as of 19:43, 24 October 2011

Publications in the MiPMap
Endlicher R, Kriváková P, Rauchová H, Nůsková H, Cervinková Z, Drahota Z (2009) Peroxidative damage of mitochondrial respiration is substrate-dependent. Physiol. Res. 58: 685-692.

» PMID:19093725

Endlicher R, Krivakova P, Rauchova H, Nuskova H, Cervinkova Z, Drahota Z (2009) Physiol. Res.

Abstract: The concentration-dependence of tert-butyl hydroperoxide (BHP) inhibitory effect on oxygen consumption in isolated rat liver mitochondria was measured in the presence of various respiratory substrates. Strong inhibitory effect at low concentrations of BHP (15-30 microM) was found for oxoglutarate and palmitoyl carnitine oxidation. Pyruvate and glutamate oxidation was inhibited at higher concentrations of BHP (100-200 microM). Succinate oxidation was not affected even at 3.3 mM BHP. Determination of mitochondrial membrane potential has shown that in the presence of NADH-dependent substrates the membrane potential was dissipated by BHP but was completely restored after addition of succinate. Our data thus indicate that beside peroxidative damage of complex I also various mitochondrial NADH-dependent dehydrogenases are inhibited, but to a different extent and with different kinetics. Our data also show that succinate could be an important nutritional substrate protecting hepatocytes during peroxidative damage. Keywords: liver mitochondria, mitochondrial enzymes, peroxidative damage, tert-butyl hydroperoxide

O2k-Network Lab: CZ_Hradec Kralove_Cervinkova Z, CZ Prague Houstek J


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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