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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Free erythrocyte porphyrin:hemoglobin (FEP:Hb) ratios were determined on 20 infants with iron-deficiency anemia. FEB:Hb ratios were compared with simultaneously drawn serum ferritin and serum transferrin saturation levels. FEP:Hb ratios dropped steadily during treatment of the anemic infants, but remained elevated compared to age-matched nonanemic infants, until the anemia was corrected. FEP:Hb ratios detected iron deficiency when acute inflammatory disease was present. Serum ferritin levels and transferrin saturation failed to detect iron deficiency after iron therapy was started or when acute inflammatory disease was present. Measurement of FEP:Hb ratios is a reliable and practical way to make a prompt diagnosis of iron-deficiency anemia in infants.
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PMID:Free erythrocyte porphyrin: hemoglobin ratios, serum ferritin, and transferrin saturation levels during treatment of infants with iron-deficiency anemia. 83 52

Fifty piglets from birth to 14 days of age were used to investigate iron binding substances of neonatal intestinal mucosa, and to evaluate the effects of these substances in neonatal iron absorption. 59Fe-labeled ferric citrate with a molecular weight of 1,500 was injected directly into the ligated duodenum. Approximately 65% of radioiron in the whole homogenate of scraped intestinal mucosa was precipitate by centrifugation for 30 minutes at 10,000 X g. Over 70% of the radioiron of the supernatant applied to Sephadex G-200 column was eluted and separated into three radioiron fractions. These iron binding substances were identified as ferritin, transferrin and a low molecular weight form by elution characteristics on chromatography and by immunological technique. Although ferritin radioactivity was the major fraction of peak 1 (73%), transferrin activity was only 54% of the whole radioiron of peak 2. The sodium dodecyl sulfate (SDS) extract of saline insoluble particles from the mucosa applied to Sepharose 4B column eluted as a single peak near the point corresponded with the ferritin peak. Although the ferritin peak contained a higher percentage of the 59Fe than the transferrin peak at birth, the percentage of ferritin decreased and percentage of transferrin increased with age. A SDS soluble iron binding substance was found in the insoluble particles of mucosa of newborn as well as nursing piglets. Since SDS, as well as saline soluble, iron binding proteins were detected in the newborn intestinal mucosa, neonatal cell membrane and cytoplasma may have an active iron transfer system. Thus, it seems likely that neonatal mucosal cell has two active iron transport mechanisms: endocytosis and transport across the plasma membrane.
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PMID:Iron binding substances in the intestinal mucosa of neonatal piglets. 84 85

A Triton X-100 solubilized macromolecular complex of transferrin and a membrane constituent can be isolated by gel chromatography from rabbit reticulocytes previously incubated with 125I-labeled transferrin. The apparent molecular weight of this complex is close to that of ferritin, or about 445 000. On sodium dodecyl sulfate gel electrophoresis the complex displays two glycoprotein subunits, of molecular weights 176 000 and 95 000 in addition to transferrin. A transferrin-binding fraction with a molecular weight near 400 000, containing these subunits, can also be identified in membranes of nonincubated reticulocytes. The corresponding membrane fraction from mature erythrocytes, which have lost transferrin-binding activity, displays both protein subunits, but the 176 000 molecular weight component fails to give a PAS stain for carbohydrate. Treatment of reticulocytes with Pronase, which destroys the ability of the cells to form specific complexes with transferrin, degrades both components. We believe these results are consistent with the hypothesis that the primary transferrin receptor of the rabbit reticulocyte is a glycoprotein of molecular weight in the range 350 000-400 000, comprised of a combination of two subunits with molecular weights 176 000 and 95 000, respectively. Transferrin-binding activity appears to depend on the carbohydrate moiety of the 176 000 subunit.
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PMID:Transferrin receptor of the rabbit reticulocyte. 84 17

We studied five patients with clinically manifest hemochromatosis and 19 of their siblings and children to define better the diagnostic criteria for stages of the disease. The earliest detectable abnormalities were an increase in hepatic-parenchymal-cell stainable iron, hepatic iron concentration, transferrin saturation and serum iron concentration. In contrast, urinary iron excretion after deferoxamine and serum ferritin concentration were usually normal in early iron loading. In either latent or clinically manifest disease, hepatic-parenchymal-cell stainable iron was Grade 3 or 4; hepatic iron concentration was greater than 250 microng per 100 mg; serum iron was greater than 170 microng per 100 ml; transferrin saturation was greater than 70 per cent; urinary iron excretion exceeded 2.2 mg per 24 hours; and serum ferritin usually exceeded 1000 ng per ml. Estimation of liver iron is the most sensitive method for detecting early disease. Urinary iron excretion and serum ferritin estimate the total body burden of iron in latent and clinically manifest disease.
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PMID:Hereditary hemochromatosis. Diagnosis in siblings and children. 86 66

The mouse with X-linked anaemia [sla] has a defect in iron absorption which can be temporarily reversee by feeding a low iron diet. Duodenal non-haem iron was significantly higher in the sla than in the normal mouse on an iron supplemented diet but non-haem iron was reduced to minute amounts when the mice were fed a low iron diet. Gel chromatography on Sephadex G-200 of th partial-free supernatant of pooled mucosal homogenates revealed the presence of three proteins binding 59Fe. Fraction I [mol wt 450 000] resembled ferritin and was present in both normal and sla mice fed an iron supplemented diet. Fraction II [mol wt 78 ooo] eluted in a similar position to transferrin and was evident in both normal and sla mice fed an iron deficient diet. Fraction III [mol wt less than 15 000] contained equivalent amounts of radioiron in normal and sla mice fed the iron deficient diet, whereas this fraction contained less radioactivity in sla animals in two of three experiments in which the animals were fed an iron supplemented diet. The iron transport defect in sla mice does not appear to reside in the iron-binding proteins in the supernatant fraction of the intestinal mucosa and the cause of the defect in iron absorption remains to be elucidated.
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PMID:Mucosal iron-binding proteins in mice with X-linked anaemia. 87 1

Ffty asymptomatic members of a kindred with familial hemochromatosis were studied in an effort to clarify some of the physiologic abnormalities present in the pre-cirrhotic or latent stage of the disease. Using excess hepatic iron as a marker for inheritance of hemochromatosis, results of liver biopsies on 31 family members suggest an auto-somal dominant mode of inheritance with incomplete expressivity. In addition to a relationship between alcohol intake and excess liver iron, there was a strong association between the level of alcohol intake and the presence of hepatic fibrosis in those subjects with excess iron stores. Both serum iron and transferrin saturation were significantly higher in family members with iron overload than in those who were not affected. Only transferrin saturation was significantly correlated with the severity of hepatic iron deposition. Studies of glucose tolerance (OGTT, IVITT, glucose clamp studies) demonstrated a defect in carbohydrate metabolism associated with deficient insulin secretion and insulin resistance, both of which were related to the degree of hepatic iron depostion. In this kindred we have found no evidence for a contribution of inheritance to the carbohydrate intolerance of hemochromatosis. Iron overload was not related to activity of hepatic collagen proline hydroxylase or urinary excretion of peptide-bound hydroxyproline. Serum ferritin, previously thought to be a reliable marker of reticuloendothelial iron stores, was normal in 19 of 20 family members with iron overload.
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PMID:Familial hemochromatosis: characteristics of the precirrhotic stage in a large kindred. 87 Jul 91

The role of iron supply in the regulation of hepatic transferrin synthesis by the isolated perfused rat liver was studied using nutritional iron deficiency as the experimental model. The increased transferrin release encountered in iron deficiency could be equated with enhanced de novo synthesis as evidenced by the inhibitory effects of cycloheximide and measurements of intrahepatic protein pools before and after perfusion. Refeeding with iron, sufficient to restore plasma iron and hepatic ferritin iron but before correction of anaemia, promoted a reduction towards normal in the transferrin synthetic rate. This effect was not produced by transfusional correction of the anaemia, suggesting a specific response to iron supply. Phenobarbitone treatment, which produced a marked fall in hepatic ferritin iron concentration but no change in haemoglobin or plasma iron concentrations, promoted a specific enhancement of transferrin synthesis in both control and iron deficient livers. The concentration of liver iron stores appears to be a major regulatory factor in the control of hepatic transferrin synthesis.
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PMID:The role of iron in the regulation of hepatic transferrin synthesis. 88 9

Human lactoferrin (Lf) labeled with 125I and/or 59Fe was found to be ingested in vitro by mouse peritoneal macrophages (MPM). The uptake measured after 15 h incubation reached a saturation point at a concentration of 200 microgram/ml in the culture medium, whatever was the iron content of Lf. In such conditions, the uptake of transferrin (Tf) used as a control was 10 times lower. At a concentration of 80 microgram/ml in the medium, one cell picked up about 0.7 X 10(6) molecules of Lf per hour, and 0.13 X 10(6) molecules of Tf per hour. Iron-saturated Lf disappeared from MPM with a half life of 14.5 h, whereas the halflife of iron-free Lf was 4.2 h. Concomitant with the intracellular digestion of Lf, the iron was transmitted to ferritin. These data provide additional support for the hypothesis that Lf plays a key role in iron turnover, especially at the level of the reticuloendothelial system where iron is recovered from the catabolism of erythrocytes.
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PMID:The ingestion and digestion of human lactoferrin by mouse peritoneal macrophages and the transfer of its iron into ferritin. 89 89

A group of 359 healthy children and 49 adults were studied for the purpose of estimating the normal limits for serum iron concentration and transferrin saturation. The 144 children and seven adults who has any other laboratory evidence of iron deficiency (abnormal values of serum ferritin, free erythrocyte protoporphyrin, hemoglobin concentration, or mean corpuscular volume) were excluded. In evaluating the 215 children and 42 adults who met the criteria to be considered normal we found that serum iron concentration and transferrin saturation were significantly lower in children between the ages of 0.5 and 12 years than in adults. We conclude that in children between the ages of 0.5 and 12 years, a transferrin saturation of less than 16% constitutes good evidence of iron deficiency only in conjuction with anemia and low mean corpuscular volume.
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PMID:Serum iron concentration and transferrin saturation in the diagnosis of iron deficiency in children: normal developmental changes. 92 12

Iron deficiency is a frequent complication in chronically hemodialyzed patients because of the significant blood losses associated with this technique. Quantitating iron stores (by marrow examination or serum iron and total iron-binding capacity) on a repetitive basis had been difficult or unreliable, often resulting in failure to recognize iron deficiency superimposed on the existing anemia of chronic renal failure, or overtreating, which can lead to iron excess. Use of the serum ferritin allows easier quantitation of iron stores and, when measured serially in dialysis patients, can predict the emergence of iron deficiency. There was no correlation between serum ferritin levels and serum iron, total iron-binding capacity, or percent transferrin saturation. Iron absorption studies show that food iron absorption is physiologic, increasing when the serum ferritin is below 30 ng/ml, decreasing when more than 300 ng/ml. Treatment of iron deficiency with oral iron compounds increases serum ferritin levels and usually can maintain iron balance.
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PMID:Iron balance in hemodialysis patients. 93 Dec 7


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