[Functional activity of mitochondria in experimental hypoparathyroidism].
Respiration and oxidative phosphorylation of the brain and hepatic mitochondria, as well as the activity of succinate dehydrogenase, succinate-cytochrome-c-reductase and cytochrome oxydase were studied in experimental hypoparathyrosis. Activated respiration and decreased effectiveness of the brain and hepatic mitochondrial phosphorylation and enhanced succinate dehydrogenase activity are seen during hypoparathyrosis development. It is suggested that alterations in mitochondrial functional activity are caused not only by the changed blood calcium ion number, but also by hypoxia, developing in experimental hypoparathyrosis.
D000818:Animals; D001921:Brain / Q000648:ultrastructure*; D003576:Electron Transport Complex IV / Q000378:metabolism; D007011:Hypoparathyroidism / Q000473:pathology*; D008297:Male; D008928:Mitochondria / Q000378:metabolism*; D008930:Mitochondria, Liver / Q000378:metabolism*; D010085:Oxidative Phosphorylation; D010101:Oxygen Consumption; D051381:Rats; D013384:Succinate Cytochrome c Oxidoreductase / Q000378:metabolism; D013385:Succinate Dehydrogenase / Q000378:metabolism
D013384:Succinate Cytochrome c Oxidoreductase; D013385:Succinate Dehydrogenase; D003576:Electron Transport Complex IV
Funktsional'naia aktivnosti' mitokhondriĭ pri éksperimental'nom gipoparatireoze.