title: Mitochondrial NADH dehydrogenase in iron-deficient and iron-repleted rat muscle: an EPR and work performance study.
abstract: Iron may affect both respiratory O2 transport and mitochondrial electron transport in the performance of muscle work. This study was designed to elucidate the molecular defect of iron-deficient work performance by identifying heretofore unmeasurable mitochondrial enzymes that are diminished by iron deficiency and may be restored by iron repletion. Female rats were made iron-deficient by dietary control and were repleted by oral iron. Iron deficiency reduced physical work capacity (treadmill running time), haemoglobin (Hb), and mitochondrial iron-sulphur (Fe-S) centres in heart and skeletal muscles; mitochondrial number was unaffected. Oral iron supplementation restored work capacity and Hb within 4 d to normal or near-normal levels, but in general Fe-S centres of mitochondria due to NADH dehydrogenase remained at iron-deficient levels. Subnormal concentrations of mitochondrial iron-dependent NADH dehydrogenase in muscle are not by themselves rate-limiting in work performance.
mesh_terms: D000747:Anemia, Hypochromic / Q000188:drug therapy / Q000201:enzymology*; D000818:Animals; D001835:Body Weight; D003579:Cytochrome Reductases / Q000378:metabolism*; D004578:Electron Spin Resonance Spectroscopy; D005260:Female; D007501:Iron / Q000627:therapeutic use; D008931:Mitochondria, Muscle / Q000201:enzymology*; D009245:NADH Dehydrogenase / Q000378:metabolism*; D005082:Physical Exertion; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D007501:Iron; D003579:Cytochrome Reductases; D009245:NADH Dehydrogenase