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Query: UMLS:C0162316 (iron deficiency anemia)
 3,806 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severe iron deficiency anemia in rats causes a decrease in the activities of iron-containing enzymes in skeletal muscle mitochondria, and subsequent diminished respiratory activity has been linked to lowered work capacity. It was suggested that loss of mitochondrial alpha-glycerophosphate dehydrogenase activity plays a particularly important role in this process and, by inference, in the clinical manifestations of iron deficiency anemia. This view may be ill founded, inasmuch as other pathways with potentially greater activity are capable of transporting reducing equivalents from the cytosol into the mitochondria in mammalian skeletal muscle. In our experiments, iron deficiency anemia of a severity on the order of that in humans was produced in guinea pigs. Mitochondria from skeletal muscles of test animals exhibited respiration rates diminished by 24% to 36% compared with control mitochondria in the presence of several substrates. However, differences in respiration were not observed with alpha-glycerophosphate as substrate, nor were there differences in alpha-glycerophosphate dehydrogenase enzyme activity between mitochondria from iron-deficient and control animals. Although cytochrome oxidase activity and muscle mitochondrial protein content were the same in both groups of guinea pigs, cytochrome and flavoprotein concentrations were lower in mitochondria from iron-deficient animals and there was a preferential loss of cytochrome c + c1. Iron deficiency anemia in guinea pigs thus results in impaired oxygen metabolism in skeletal muscle mitochondria that is associated with a general decrease in the concentrations of iron-containing electron transport chain components as well as with an alteration in chain stoichiometry.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Iron deficiency anemia: mitochondrial alpha-glycerophosphate dehydrogenase in guinea pig skeletal muscle. 298 41

The purpose of this study was to determine the interrelationships between iron stores, serum iron, hemoglobin, myoglobin, and cytochrome c under conditions of iron deficiency that did not interfere with normal growth. Rats were given diets containing from 7 to 500 mg iron per kilogram of diet during a period of 3 weeks of rapid growth between weaning at 21 days and approaching sexual maturity at 42 days. We found that the level of iron intake required for a maximum concentration of hemoglobin was similar to that which results in a maximum level of tissue cytochrome c. The severity of iron deficiency anemia was proportionally similar to the degree of depletion of muscle cytochrome c at all levels of iron intake below 25 mg/kg diet. The results indicate that even the mildest degree of nutritional iron deficiency anemia also affected tissue cytochrome c and could impair cytochrome-dependent mitochondrial function.
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PMID:Manifestation of iron deficiency at various levels of dietary iron intake. 624 52