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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hemoglobin and myoglobin are a major source of dietary iron in man. Heme, separated from these hemoproteins by intraluminal proteolysis, is absorbed intact by the intestinal mucosa. The absorbed heme is cleaved in the mucosal cell releasing inorganic iron. Although this mucosal heme-splitting activity initially was ascribed to xanthine oxidase, we investigated the possibility that it is catalyzed by microsomal heme oxygenase, an enzyme which converts heme to bilirubin, CO, and inorganic iron. Microsomes prepared from rat intestinal mucosa contain enzymatic activity similar to that of heme oxygenase in liver and spleen. The intestinal enzyme requires NADPH; is completely inhibited by 50% CO; and produces bilirubin IX-alpha, identified spectrophotometrically and chromatographically. Moreover, duodenal heme oxygenase was shown to release inorganic (55)Fe from (55)Fe-heme. Along the intestinal tract, enzyme activity was found to be highest in the duodenum where hemoglobin iron absorption is reported to be most active. Furthermore, when rats were made iron deficient, duodenal heme oxygenase activity and hemoglobin-iron absorption rose to a comparable extent. Upon iron repletion of iron-deficient animals, duodenal enzyme activity returned towards control values. In contrast to heme oxygenase, duodenal xanthine oxidase activity fell sharply in iron deficiency and rose towards base line upon iron repletion. Our findings suggest that mucosal heme oxygenase catalyzes the cleavage of heme absorbed in the intestinal mucosa and thus plays an important role in the absorption of hemoglobin iron. The mechanisms controlling this intestinal enzyme activity and the enzyme's role in the overall regulation of hemoglobin-iron absorption remain to be defined.
J Clin Invest 1974 Dec
PMID:Intestinal absorption of hemoglobin iron-heme cleavage by mucosal heme oxygenase. 443 36

The importance of ceruloplasmin in iron metabolism was studied in swine made hypoceruloplasminemic by copper deprivation. When the plasma ceruloplasmin level fell below 1% of normal, cell-to-plasma iron flow became sufficiently impaired to cause hypoferremia, even though total body iron stores were normal. When ceruloplasmin was administered to such animals, plasma iron increased immediately and continued to rise at a rate proportional to the logarithm of the ceruloplasmin dose. The administration of inorganic copper induced increases in plasma iron only after ceruloplasmin appeared in the circulation. Thus, ceruloplasmin appeared to be essential to the normal movement of iron from cells to plasma. Studies designed to define the mechanism of action of ceruloplasmin were based on the in vitro observation that ceruloplasmin behaves as an enzyme (ferroxidase) that catalyzes oxidation of ferrous iron. Retention of injected ferrous iron in the plasma of ceruloplasmin-deficient swine was significantly less than that of ferric iron, reflecting impaired transferrin iron binding. Rat ceruloplasmin, which has little ferroxidase activity, was much less effective than porcine or human ceruloplasmin in inducing increases in plasma iron. These observations suggest that ceruloplasmin acts by virtue of its ferroxidase activity. Eight patients with Wilson's disease were evaluated in order to investigate iron metabolism in a disorder characterized by reduced ceruloplasmin levels. Evidence of iron deficiency was found in six of these, and in five of the six, plasma ceruloplasmin was less than 5% of normal. In comparison, the two patients without evidence of iron deficiency had ceruloplasmin levels of 11 and 18% of normal. It is suggested that iron deficiency tends to occur in those patients with Wilson's disease who have the severest degrees of hypoceruloplasminemia, possibly because of defective transfer of iron from intestinal mucosal cells to plasma.
J Clin Invest 1970 Dec
PMID:The role of ceruloplasmin in iron metabolism. 548 Aug 64

The role of heme in the synthesis of cytochrome c oxidase has been investigated in the mold Neurospora crassa. Iron-deficient cultures of the mold have low levels of cytochrome oxidase and delta-aminolevulinate dehydratase, the latter being the rate-limiting enzyme of the heme-biosynthetic pathway in this organism. Addition of iron to the iron-deficient cultures results in an immediate increase in the levels of delta-aminolevulinate dehydratase followed by an increase in the rate of heme synthesis and cytochrome oxidase levels. The rate of precursor labeling of the mitochondrial subunits of cytochrome oxidase is decreased preferentially under conditions of iron deficiency and addition of iron corrects this picture. Exogenous hemin addition which prevents iron-mediated induction of delta-aminolevulinate dehydratase also inhibits the increase in the activity of cytochrome oxidase and the enhanced precursor labeling of the mitochondrial subunits of cytochrome oxidase. Protein synthesis on mitoribosomes measured in vivo and in vitro is decreased under conditions of heme deficiency. Hemin addition in vitro to mitochondrial lysates prepared from heme-deficient mycelia restores a near normal rate of protein synthesis. It is concluded that heme is required for the optimal rate of translation on mitoribosomes.
J Biol Chem 1980 Dec 10
PMID:Role of heme in the synthesis of cytochrome c oxidase in Neurospora crassa. 625 61

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.
Br J Haematol 1982 Dec
PMID:Mitochondrial NADH dehydrogenase in iron-deficient and iron-repleted rat muscle: an EPR and work performance study. 629 76

In this study of 467 healthy term infants seen for routine 1-year health maintenance examination, we determined the influence of mild prior infection on the concentration of hemoglobin and other laboratory evidence of iron deficiency. In addition we studied the Hgb response in 261 infants randomized to receive a 3-month course of treatment with either iron or placebo. Infants who had had one or more clinic visits because of infection during the previous 3 months or who were reported as not being entirely well during the past month or who had an elevated sedimentation rate were more likely to have anemia or "low normal" Hgb, higher erythrocyte protoporphyrin and serum ferritin values, and lower serum iron concentration than infants who had been well. Hgb response greater than or equal to 1 gm/dl after iron treatment occurred more commonly in infants who had had prior visits because of infection. The results indicate that upper respiratory and other mild antecedent infections commonly predispose to iron deficiency (probably because of a decrease in iron absorption).
J Pediatr 1984 Dec
PMID:Iron deficiency in infants: the influence of mild antecedent infection. 650 35

Serum iron, serum transferrin and transferrin saturation were studied in 253 healthy, non-anaemic children 4, 8 and 13 years old, and in 60 healthy, non-anaemic adults having serum ferritin values greater than or equal to 15 micrograms/l. One hundred and ninety-six children had serum ferritin values greater than or equal to 15 micrograms/l (i.e. replete iron stores), 35 had intermediate ferritin values from 10-14 micrograms/l and 22 had ferritin values less than 10 micrograms/l (i.e. depleted iron stores). Iron replete children showed a gradual rise in serum iron and transferrin saturation values with age. Serum iron and transferrin saturation values were lower (P less than 0.001, P less than 0.0001) and transferrin values higher (P less than 0.0001) in iron replete children compared to adults. Iron replete children had a 2.5 centile transferrin saturation value of 5%; 19.9% of these children had saturation values less than 15% and 8.2% had values less than 10%. In iron depleted children a transferrin saturation value less than 7% yielded the highest diagnostic efficiency as regards exhausted iron stores, although with a low predictive value of a positive test. The transferrin saturation is unsuitable as a single diagnostic criterion in the evaluation of iron deficiency in children and should always be combined with other indicators of iron status.
Eur J Pediatr 1984 Dec
PMID:Serum iron, serum transferrin and transferrin saturation in healthy children without iron deficiency. 651 18

Two experiments were performed to investigate the effect of dietary iron deficiency during reproduction on folate status in rat dams and pups. In experiment 1, twenty pregnant Sprague-Dawley rats (190-200 g) were fed one of two diets (8 ppm Fe, 1 ppm folate or 250 ppm Fe, 1 ppm folate) throughout gestation and until day 18 of lactation when dams and their pups (seven per litter) were killed. Although there was no effect of iron deficiency on dam folate status, iron-deficient pups had decreased liver folate activity compared to controls. Milk free folate activity was significantly decreased by 34% in iron-deficient dams compared to controls. To determine if iron deficiency affected folate status at birth, experiment 2 was conducted. Nine pregnant rats (215-230 g) were fed one of two diets (6 ppm Fe, 1 ppm folate or 250 ppm Fe, 1 ppm folate) throughout gestation and until day 2 of lactation. Liver and kidney folate activities were similar in both groups of pups on day 2 of lactation. It is concluded that the stress of lactation superimposed on iron deficiency alters the folate composition of rat milk, and results in folate depletion in 18-day-old rat pups.
J Nutr 1983 Dec
PMID:Folate depletion secondary to iron deficiency in the neonatal rat. 665 11

Although iron deficiency is not recognized as a usual complication of hemophilia, we questioned whether intermittent occult loss of blood in urine or stool might predispose hemophiliacs to chronic iron deficiency. Seven men with factor VII and one with factor IX deficiency were studied. Blood studied, bone marrow aspirates, urine and stool samples, and ferrokinetics with total-body counting up to five months were examined. These data showed no excessive loss of blood during the study period; however, marrow iron stores were decidedly decreased, being absent in four subjects. We suggest that in some hemophiliacs, iron deposits in tissues such as synovial membranes may form a high proportion of the body's total iron stores.
Arch Pathol Lab Med 1981 Dec
PMID:Iron studies in hemophilia. 689 54

This article reviews selected nutrition research pertinent to adolescent health care. Protein--calorie malnutrition affects 25% of hospitalized adolescents studied, which correlates, as in adults, with increased morbidity and mortality. Some subgroups of adolescents, notably Asian immigrants, have been shown to be at high risk for developing vitamin D deficient rickets. On the other hand, excessive vitamin D intake has been linked to arteriosclerosis in animal models. Calcium supplementation is not likely to be indicated in U.S. adolescents. Iron deficiency prevalence in adolescence is not well documented, owing to the confusion between anemia and iron deficiency. Serum ferritin and free erythrocyte protoporphyrin measures should help to clarify this issue. Zinc nutrition must be assessed in high-risk groups such as those with short stature or Crohn's disease. Oral contraception effects on vitamin B6 and on serum lipids need to be considered in the risk-benefit equation when prescribing this method of birth control for adolescents.
J Adolesc Health Care 1980 Dec
PMID:Nutrition and the adolescent: an update. 702 6

We made direct noninvasive magnetic measurements of hepatic iron stores with a specially designed superconducting quantum-interference-device (SQUID) susceptometer in 20 normal subjects and in 110 patients with liver disease, iron deficiency, hereditary hemochromatosis, or transfusional iron overload. Magnetic in vivo measurements of liver non-heme iron were closely correlated with chemical in vitro measurements in liver-biopsy specimens (r = 0.98, P less than 10(-5) up to 115 mumol per gram of liver tissue (wet weight) or more. Magnetically determined storage-iron concentrations were below 6.0 mumol per gram in iron-deficient patients and normal men and premenopausal women, but they were raised (9.7 to 31.4 mumol) in 12 of 67 patients with liver disease and were greatly increased (22.9 to 117.7 mumol) in patients with untreated hereditary hemochromatosis or transfusional iron overload. Magnetic measurements of iron stores provide a new quantitative technique for early detection of hereditary hemochromatosis and for rapid evaluation of treatment regimens for transfusional iron overload.
N Engl J Med 1982 Dec 30
PMID:Magnetic-susceptibility measurement of human iron stores. 714 66


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