Mitochondrial NADH dehydrogenase in iron-deficient and iron-repleted rat muscle: an EPR and work performance study.
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.
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
D007501:Iron; D003579:Cytochrome Reductases; D009245:NADH Dehydrogenase