Effect of iron deficiency on energy conservation in rat liver and skeletal muscle submitochondrial particles.
Submitochondrial particles prepared from liver and skeletal muscle of control and iron-deficient rats were examined for cytochrome content and for both energy-independent and energy-conserving functions. Liver submitochondrial particles appear quite resistant to iron deficiency with cytochrome content and electron-transferring or energy-conserving functions maintained at a level of 85% or better of normal. Iron-deficient skeletal muscle submitochondrial particles, in contrast, have decreased cytochrome content and only 15-20% of the normal capacity for oxidation through either complex I (NADH dehydrogenase) or complex II (succinate dehydrogenase). Energy-linked reactions which involve substrate oxidation/reduction (succinate----NAD+ reversed electron flow and succinate-driven energy-dependent transhydrogenation) are likewise markedly decreased, while ATP-driven energy-dependent transhydrogenation and mitochondrial ATPase are normal. Our data support the concept that iron deficiency leads to decreased electron-carrying capacity of iron-containing mitochondrial enzymes, with skeletal muscle being much more susceptible than liver, but that the mitochondria are otherwise normal with regard to energy conservation.
D000227:Adenine Nucleotides / Q000378:metabolism; D000818:Animals; D003580:Cytochromes / Q000378:metabolism; D004579:Electron Transport; D004734:Energy Metabolism; D000090463:Iron Deficiencies; D008930:Mitochondria, Liver / Q000378:metabolism*; D008931:Mitochondria, Muscle / Q000378:metabolism*; D009243:NAD / Q000378:metabolism; D051381:Rats; D013367:Submitochondrial Particles / Q000378:metabolism; D013386:Succinates / Q000378:metabolism; D019802:Succinic Acid
D000227:Adenine Nucleotides; D003580:Cytochromes; D013386:Succinates; D009243:NAD; D019802:Succinic Acid