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Difference between revisions of "Kasparova 2006 Neurochem Int"

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{{Publication
{{Publication
|title=Kasparova S, Sumbalova Z, Bystricky P, Kucharska J, Liptaj T, Mlynarik V, Gvozdjakova A (2006) Effect of coenzyme Q10 and vitamin E on brain energy metabolism in the animal model of Huntington's disease. Neurochem Int 48(2):93-9.
|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 the pseudo-first order rate constant (k(for)) of the forward CK reaction, the
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)
phosphocreatine (PCr) to adenosinetriphosphate (ATP) ratio, intracellular pH(i)
and Mg(i)(2+) content in the brain. The respiratory chain function of isolated
and Mg(i)(2+) content in the brain. The respiratory chain function of isolated
Line 24: Line 22:
CoQ(10)+vitamin E prevented increase of k(for) and the decrease of CoQ(10)
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
content in brain tissue, but were ineffective to prevent the decline of
respiratory chain function. We suppose that increased activity of CK system could
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.
be compensatory to decreased mitochondrial ATP production, and CoQ(10)+vitamin E  
|keywords=Creatine kinase, ''In vivo'' saturation transfer 31P NMR, Rats, 3-Nitropropionic acid, Oxidative phosphorylation, Antioxidants
could prevent the increase of k(for) after 3-NP treatment likely by activity of
|mipnetlab=SK Bratislava Sumbalova Z
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
|discipline=Mitochondrial Physiology
|discipline=Mitochondrial Physiology
}}
}}
{{Labeling
{{Labeling
|injuries=Mitochondrial Disease; Degenerative Disease and Defect
|injuries=Mitochondrial disease
|organism=Rat
|organism=Rat
|tissues=Neurons; Brain
|tissues=Nervous system
|preparations=Intact Organism, Isolated Mitochondria
|preparations=Intact organism, Isolated mitochondria
|topics=Respiration; OXPHOS; ETS Capacity, ATP; ADP; AMP; PCr
|topics=ATP
|couplingstates=OXPHOS
|additional=Huntington´s disease
|additional=Huntington´s disease
|discipline=Mitochondrial Physiology
|discipline=Mitochondrial Physiology
}}
}}

Latest revision as of 15:42, 27 March 2018

Publications in the MiPMap
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.

» PMID: 16290265

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

• O2k-Network Lab: SK Bratislava Sumbalova Z


Labels:

Stress:Mitochondrial disease  Organism: Rat  Tissue;cell: Nervous system  Preparation: Intact organism, Isolated mitochondria 

Regulation: ATP  Coupling state: OXPHOS 


Huntington´s disease 

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