Asunto(s)
Granulocitos , Leucemia Mieloide Aguda/terapia , Leucemia Mieloide/patología , Recuento de Células Sanguíneas , Transfusión de Sangre Autóloga , Médula Ósea/patología , Estudios de Seguimiento , Humanos , Leucemia Mieloide/sangre , Leucemia Mieloide Aguda/sangre , Masculino , Persona de Mediana EdadRESUMEN
We have examined the effects of total body iron deficiency on the function of mitochondria isolated from rat hearts. Male Wistar rats were weaned at 21 days and divided into an experimental iron-deficient group and a control group. Both groups received identical diet but an iron supplement (180 mg of ferrous sulfate per kg of diet) was added for the control group. Rats were studied at 7 and 14 weeks. Iron-deficient rats weighed less than controls but showed significantly increased ventricle to body weight ratio at both 7 and 14 weeks, indicating relative cardiac hypertrophy. Isolated mitochondrial fractions from iron-deficient and control rats contained similar proportions of whole homogenate protein and succinic cytochrome c reductase activity, indicating that the fractions isolated from the experimental and control rats were comparable. In iron-deficient rats NADH cytochrome c reductase, succinic cytochrome c reductase, succinic dehydrogenase, and NADH ferricyanide oxidoreductase activities were all significantly reduced at 7 and 14 weeks. Cytochrome c oxidase activity was significantly reduced only at 14 weeks as were the concentrations of cytochromes a3, c1, and b. The rate of oxygen uptake by mitochondria was significantly lower at both 7 and 14 weeks but the P/O ratio was unaltered. We conclude that iron deficiency is associated with impairment of myocardial mitochondrial electron transport.
Asunto(s)
Anemia Hipocrómica/metabolismo , Grupo Citocromo c/metabolismo , Miocardio/metabolismo , Consumo de Oxígeno , Anemia Hipocrómica/enzimología , Animales , Peso Corporal , Cardiomegalia/metabolismo , Reductasas del Citocromo/metabolismo , Complejo IV de Transporte de Electrones/metabolismo , Masculino , Mitocondrias Musculares/metabolismo , Miocardio/enzimología , NADPH-Ferrihemoproteína Reductasa/metabolismo , Fosforilación Oxidativa , Ratas , Succinato Deshidrogenasa/metabolismoRESUMEN
1. The observation that thyroid C cell hyperplasia occurred in rats given the iron-deficient diet described by McCall, Newman, O'Brien, Valberg & Witts (1962) prompted a closer study of the preparation and constituents of this diet. 2. It became apparent that there was a discrepancy between the amounts of fat-soluble vitamins in the dietary formulation reported and the supposed final content of the diet. A diet prepared as described by McCall et al. (1962) contains 1000 mug (40 000 i.u.) ergocalciferol and 10 mug (14 500 i.u.) retinyl palmitate/kg. 3. An experiment was designed to study the effect of Fe-deficient and Fe-supplemented, high-vitamin-D diets, and an Fe-supplemented, normal-vitamin-D diet, on thyroid C cell volume and serum calcium concentration. 4. Thyroid C cell volumes and serum Ca concentrations were significantly higher in both groups given excess vitamin D than in the group given the Fe-supplemented, normal-vitamin-D diet. It is evident therefore, that hypervitaminosis D was the cause of the morphological and biochemical changes found in rats given the McCall et al. (1962) diet.