The influence of thyroid hormone on the degree of control of oxidative phosphorylation exerted by the adenine nucleotide translocator.
Impaired phosphorylation efficiency in liver mitochondria from hypothyroid rats is paralleled by a defect in adenine nucleotide transport. Both of these lesions can be corrected within 15 min by a near-physiological dose of triiodo-L-thyronine. Measurement of the control strength of the translocator shows, however, that this step has a smaller share of the control for oxidative phosphorylation after thyroidectomy and that this is unaltered after 15 min by replacement therapy. Rapid control by triiodothyronine is thus exerted elsewhere than at this transfer and the effects of hormone on the translocator are likely to be indirect.
D000818:Animals; D001278:Atractyloside / Q000031:analogs & derivatives / Q000494:pharmacology; D007037:Hypothyroidism / Q000378:metabolism*; D007700:Kinetics; D008297:Male; D008930:Mitochondria, Liver / Q000187:drug effects / Q000378:metabolism*; D000226:Mitochondrial ADP, ATP Translocases / Q000378:metabolism*; D009713:Nucleotidyltransferases / Q000378:metabolism*; D010085:Oxidative Phosphorylation / Q000187:drug effects*; D051381:Rats; D013965:Thyroidectomy; D014284:Triiodothyronine / Q000494:pharmacology*
D014284:Triiodothyronine; D001278:Atractyloside; D000226:Mitochondrial ADP, ATP Translocases; D009713:Nucleotidyltransferases; C003853:carboxyatractyloside