Brain ATP Metabolism in Hypoxia Resistant Mice Fed Guanidinopropionic Acid
Autor: | Eddie O'Gorman, David Holtzman, M. Brown, Theo Wallimann, Elizabeth N. Allred |
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Rok vydání: | 1998 |
Předmět: |
medicine.medical_specialty
Guanidinopropionic acid Drug Resistance Adenylate kinase Mice Inbred Strains Creatine transport macromolecular substances Guanidines Potassium Chloride Rats Sprague-Dawley Mice chemistry.chemical_compound Adenosine Triphosphate Oxygen Consumption stomatognathic system Developmental Neuroscience Internal medicine medicine Animals Hypoxia Creatine Kinase biology Respiration Adenylate Kinase Brain ATP metabolism Hypoxia (medical) Mitochondria Rats Adenosine Diphosphate Sprague dawley Endocrinology Neurology chemistry biology.protein Female Oligomycins Creatine kinase Propionates medicine.symptom Competitive inhibitor |
Zdroj: | Developmental Neuroscience. 20:469-477 |
ISSN: | 1421-9859 0378-5866 |
DOI: | 10.1159/000017345 |
Popis: | Feeding β-guanidinopropionic acid (GPA), a competitive inhibitor of creatine transport, decreases mortality and increases brain ATP stability in hypoxic mice. To study brain ATP metabolism in GPA-fed animals, respiratory rates were measured in grey matter and white matter slices as well as cerebral hemisphere mitochondria from GPA-fed mice and rats. Creatine kinase and adenylate kinase activities were measured in rat cerebral grey matter and white matter. Respiratory rates and oxidative phosphorylation were the same in GPA-fed mice and control mice. The adenylate kinase activity increased 50% and creatine kinase showed a small decrease in grey matter. In white matter, creatine kinase increased 50% while adenylate kinase decreased. Thus, GPA produces opposite adaptive changes in adenylate kinase and creatine kinase in grey matter and in white matter. These results suggest that the creatine kinase reaction in grey matter acts to regulate cellular ADP and ATP concentrations. |
Databáze: | OpenAIRE |
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