An animal model of mitochondrial myopathy: a biochemical and physiological investigation of rats treated in vivo with the NADH-CoQ reductase inhibitor, diphenyleneiodonium
| Autor: | John B. Clark, R. K. H. Petty, M.J. Brosnan, D. J. Hayes, George K. Radda, J. A. Morgan-Hughes, E.A. Shoubridge, J. M. Cooper, R. A. J. Challiss |
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| Rok vydání: | 1988 |
| Předmět: |
Male
medicine.medical_specialty Time Factors Phosphocreatine Biology Reductase chemistry.chemical_compound Gastrocnemius muscle Onium Compounds Mitochondrial myopathy Muscular Diseases Internal medicine medicine NAD(P)H Dehydrogenase (Quinone) Animals Quinone Reductases Myopathy Muscle fatigue Dose-Response Relationship Drug Muscles Skeletal muscle Rats Inbred Strains medicine.disease Mitochondria Muscle Rats Endocrinology medicine.anatomical_structure Neurology chemistry Lactic acidosis Neurology (clinical) medicine.symptom Acidosis |
| Zdroj: | Journal of the neurological sciences. 83(2-3) |
| ISSN: | 0022-510X |
| Popis: | Chronic administration of the NADH-CoQ reductase inhibitor, diphenyleneiodonium to rats at two dose levels, 1.0 and 1.5 mg/kg per day, caused a 40% and 60% reduction, respectively, in the in vitro rate of NAD-linked respiration by skeletal muscle mitochondria. At the highest dose, muscle fatigue, lactic acidosis and an over-utilization of phosphocreatine was observed in the gastrocnemius muscle during mild stimulation of 1 Hz frequency. The resynthesis of phosphocreatine following muscle stimulation was about 2 fold slower in the treated animal group. At the low dose, no significant biochemical changes were observed during muscle stimulation at 4 Hz. The results are discussed in terms of skeletal muscle "oxidative reserve", twitch tension maintenance and the relevance to the human diseased state of mitochondrial myopathy. |
| Databáze: | OpenAIRE |
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