Difference between revisions of "Kasparova 2006 Neurochem Int"
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{{Publication | {{Publication | ||
|title= | |title=Kasparová S, Sumbalová Z, Bystrický P, Kucharská J, Liptaj T, Mlynárik V, Gvozdjáková A (2006) Effect of coenzyme Q10 and vitamin E on brain energy metabolism in the animal model of Huntington's disease. Neurochem Int 48:93-9. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/16290265 PMID: 16290265] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/16290265 PMID: 16290265] | ||
|authors=Kasparova S, Sumbalova Z, Bystricky P, Kucharska J, Liptaj T, Mlynarik V, Gvozdjakova A | |authors=Kasparova S, Sumbalova Z, Bystricky P, Kucharska J, Liptaj T, Mlynarik V, Gvozdjakova A | ||
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kinase (CK) and the function of mitochondrial respiratory chain in the brain of | kinase (CK) and the function of mitochondrial respiratory chain in the brain of | ||
aged rats administered with 3-NP with and without previous application of | aged rats administered with 3-NP with and without previous application of | ||
antioxidants CoQ(10)+vitamin E. We used dynamic and steady-state methods of in | antioxidants CoQ(10)+vitamin E. We used dynamic and steady-state methods of ''in | ||
vivo phosphorus magnetic resonance spectroscopy ((31)P MRS) for determination of | vivo'' phosphorus magnetic resonance spectroscopy ((31)P MRS) for determination of | ||
the pseudo-first order rate constant (k(for)) of the forward CK reaction, the | the pseudo-first order rate constant (k(for)) of the forward CK reaction, the | ||
phosphocreatine (PCr) to adenosinetriphosphate (ATP) ratio, intracellular pH(i) | phosphocreatine (PCr) to adenosinetriphosphate (ATP) ratio, intracellular pH(i) | ||
Line 30: | Line 30: | ||
elucidation of mechanism of beneficial effect of CoQ(10) administration in HD and | elucidation of mechanism of beneficial effect of CoQ(10) administration in HD and | ||
showed that the rate constant of CK is a sensitive indicator of brain energy | showed that the rate constant of CK is a sensitive indicator of brain energy | ||
disorder reflecting therapeutic effect of drugs that could be used as a new in | disorder reflecting therapeutic effect of drugs that could be used as a new ''in | ||
vivo biomarker of neurodegenerative diseases. | vivo'' biomarker of neurodegenerative diseases. | ||
|keywords=Creatine kinase; In vivo saturation transfer 31P NMR; Rats; 3-Nitropropionic acid; Oxidative phosphorylation; Antioxidants | |keywords=Creatine kinase; ''In vivo'' saturation transfer 31P NMR; Rats; 3-Nitropropionic acid; Oxidative phosphorylation; Antioxidants | ||
|discipline=Mitochondrial Physiology | |discipline=Mitochondrial Physiology | ||
}} | }} |
Revision as of 15:10, 30 March 2015
Kasparová S, Sumbalová Z, Bystrický P, Kucharská J, Liptaj T, Mlynárik V, Gvozdjáková A (2006) Effect of coenzyme Q10 and vitamin E on brain energy metabolism in the animal model of Huntington's disease. Neurochem Int 48:93-9. |
Kasparova S, Sumbalova Z, Bystricky P, Kucharska J, Liptaj T, Mlynarik V, Gvozdjakova A (2006) Neurochem Int
Abstract: The neuropathological and clinical symptoms of Huntington's disease (HD) can be simulated in animal model with systemic administration of 3-nitropropionic acid (3-NP). Energy defects in HD could be ameliorated by administration of coenzyme Q(10) (CoQ(10)), creatine, or nicotinamid. We studied the activity of creatine kinase (CK) and the function of mitochondrial respiratory chain in the brain of aged rats administered with 3-NP with and without previous application of antioxidants CoQ(10)+vitamin E. We used dynamic and steady-state methods of in vivo phosphorus magnetic resonance spectroscopy ((31)P MRS) for determination of the pseudo-first order rate constant (k(for)) of the forward CK reaction, the phosphocreatine (PCr) to adenosinetriphosphate (ATP) ratio, intracellular pH(i) and Mg(i)(2+) content in the brain. The respiratory chain function of isolated mitochondria was assessed polarographically; the concentration of CoQ(10) and alpha-tocopherol by HPLC. We found significant elevation of k(for) in brains of 3-NP rats, reflecting increased rate of CK reaction in cytosol. The function of respiratory chain in the presence of succinate was severely diminished. The activity of cytochromeoxidase and mitochondrial concentration of CoQ(10) was unaltered; tissue content of CoQ(10) was decreased in 3-NP rats. Antioxidants CoQ(10)+vitamin E prevented increase of k(for) and the decrease of CoQ(10) content in brain tissue, but were ineffective to prevent the decline of respiratory chain function. We suppose that increased activity of CK system could be compensatory to decreased mitochondrial ATP production, and CoQ(10)+vitamin E could prevent the increase of k(for) after 3-NP treatment likely by activity of CoQ(10) outside the mitochondria. Results of our experiments contributed to elucidation of mechanism of beneficial effect of CoQ(10) administration in HD and showed that the rate constant of CK is a sensitive indicator of brain energy disorder reflecting therapeutic effect of drugs that could be used as a new in vivo biomarker of neurodegenerative diseases. • Keywords: Creatine kinase; In vivo saturation transfer 31P NMR; Rats; 3-Nitropropionic acid; Oxidative phosphorylation; Antioxidants
Labels:
Stress:Mitochondrial disease Organism: Rat Tissue;cell: Nervous system Preparation: Intact organism, Isolated mitochondria
Regulation: ATP; ADP; AMP; PCr"ATP; ADP; AMP; PCr" 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. Coupling state: OXPHOS
Huntington´s disease