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

Male and female blood donors were grouped according to their blood donations, and the iron stores were estimated by a two-site immunoradiometric assay for ferritin. Hb serum iron, serum transferrin and transferrin saturation were also measured. A remarkable low serum ferritin concentration was found in male donors, who had donated blood one or two times. This might indicate that the serum ferritin concentration in male blood donors is not linearly correlated to the iron stores. Among 30 female donors 14 had ferritin values below 10 ng/ml, which have been shown to be indicative of iron deficiency. The serum ferritin concentration could not be used to predict the donors who developed low Hb values by the blood donation which followed. Serum ferritin was correlated to serum iron in men and to serum transferrin and transferrin saturation in both men and women.
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PMID:Iron stores in blood donors evaluated by serum ferritin. 62 33

Sheep were treated with large amounts of copper (20 mg of CuSO4,5H2O/kg body wt. per day) for 9 weeks to examine the effect of copper excess on iron metabolism. In addition to confirming that massive haemolysis and accumulation of copper occurs in the liver, kidney and plasma after 7 weeks of exposure to excess copper, it was observed that excess copper produced an increased plasma iron concentration and transferrin saturation within 1 week. Further, iron preferentially accumulated in the spleen between 4 and 6 weeks of copper treatment, producing 3-fold increases in the iron content of both the ferritin and non-ferritin fractions. A 3-4 fold increase was also observed in the amount of ferritin that could be isolated from the spleen. The copper treatment had little or no effect on the concentration of iron in the liver and bone marrow. The following properties of erythrocytes were also unaffected by copper treatment: size, haemoglobin content and pyruvate kinase activity, although the erythrocyte concentration of copper increased after 6 weeks. Copper accumulated in the spleen between 6 and 9 weeks, probably owing to the phagocytosis of erythrocytes containing high concentrations of copper. The data suggest that copper excess influences iron metabolism, initially by causing a compensated haemolytic anaemia, and later by interfering with re-utilization of iron from ferritin in the reticuloendothelial cells of the spleen.
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PMID:The effect of copper excess on iron metabolism in sheep. 62 72

The developmental changes in red blood cell counts and indices were determined in infants after mild iron deficiency was excluded. The normal values were obtained from a selected group of healthy, term infants who were receiving continuous iron supplementation during a period of one year while normal values for transferrin saturation and serum ferritin were being maintained. The data indicated marked developmental changes in red blood cell counts and indices during the first year of life that are independent of iron intake. Serial analysis of individual infant's values indicated that the red cell measurement at 4 months of age are, to some extent, predictive of the level of subsequent values within the normal range.
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PMID:Developmental changes in red blood cell counts and indices of infants after exclusion of iron deficiency by laboratory criteria and continuous iron supplementation. 63 80

1. Plasma membranes prepared by pre-incumbation of mouse reticulocytes with 125I, 59Fe-labeled murine transferrin were able to release 59Fe in preference to 125I when incubated in the presence of murine reticulocyte cytosol, demonstrating that the latter mobilized iron which had been dissociated from transferrin. 2. 59Fe in cytosol was associated with at least two components in addition to hemoglobin, a high molecular weight component, identified as ferritin by specific immunoprecipitation, and an as yet unidentified, low molecular weight component of approx 17 00. 3. Ferritin itself, in the absence of added cytosol, was abloe to mobilize 59Fe from s9Fe-labeled reticulocyte plasma membranes. 4. Lysates of reticulocytes synthesized 59Fe-labeled heme when incubated with 59Fe-labeled ferritin. 5. These findings reflect a pathway of iron uptake and incorporation into heme in which ferritin plays an active role.
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PMID:Mobilization of iron from the plasma membrane of the murine reticulocyte. The role of ferritin. 64 5

Free erythrocyte protoporphyrin (FEP) and serum ferritin have been determined in 57 healthy children and in 25 children with varying degrees of iron deficiency. FEP was found to be inversely correlated to the concentration of hemoglobin (r = -0.80) as well as to serum ferritin (r=-0.64). Elevated FEP was found in children with hemoglobin less than 12.5 g/dl, or serum ferritin less than 8 microgram/l. In a group of apparently hematologically normal children between the age of 10--14 years (hemoglobin greater than 12.5 g/dl), a 2-month-trial of iron medication resulted in an increase in hemoglobin and ferritin, and a decrease in FEP, indicating suboptimal supply of iron for hemoglobin synthesis before iron medication. In a patient with iron deficiency (FEP 15.3 mumole/l, hemoglobin 5.2 g/dl), iron therapy was followed by a rapid fall in FEP before any changes in hemoglobin, serum iron transferrin saturation and ferritin could be detected. The rapid fall in FEP during start of treatment in iron deficiency makes FEP a sensitive biochemical parameter on iron homeostasis in iron deficiency anemia.
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PMID:The diagnosis of iron deficiency by erythrocyte protoporphyrin and serum ferritin analyses. 65 13

Iron status, as measured by blood counts and indices, serum iron, transferrin saturation, and serum ferritin values, was studied longitudinally in 56 infants on prolonged breast feeding, and compared to that of 29 infants receiving cow milk formula prepared at home and of 47 infants receiving a proprietary infant formula. The first two groups received no iron supplementation, whereas the proprietary formula was supplemented with iron. Although breast feeding was found to be sufficient to meet iron needs during the first 6 months of life, supplemental iron would be necessary during the second half of infancy in order to guarantee the optimal iron status.
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PMID:Need for iron supplementation in infants on prolonged breast feeding. 67 Nov 50

The value of tests for the detection of body iron overload was investigated in 8 patients with clinically manifest primary hemochromatosis, 12 patients with cirrhosis and iron overload and 20 patients with liver disease and low or normal iron stores. Iron overload was defined as the presence of stainable iron in more than 50% of hepatocytes in a liver biopsy specimen. The percentages of patients with a true-positive (abnormal) or true-negative (normal) result were: serum iron concentration 65%, transferin saturation 85%, serum ferritin concentration 78%, serum ferritin:serum glutamic oxaloacetic transaminase (SGOT) index 78%, percent iron absorption 58%, percent iron absorption in relation to serum ferritin concentration 80% and percent iron absorption in relation to serum ferritin:SGOT index 93%. The calculated predictive value of a normal test result for the exclusion of iron overload in patients with liver disease, a group with an assumed prevalence of iron overload of 10%, was 98% to 99% for transferrin saturation and serum ferritin concentration used alone and 100% for these measures used together; the predictive value of an abnormal result for the diagnosis of iron overload was less than 50% for all of the above measures used alone or in combination. Hence, in patients with an increased serum ferritin concentration or transferrin saturation, or both, determination of the hepatocellular iron content of a specimen from a percutaneous liver biopsy is required for the diagnosis of iron overload.
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PMID:Diagnostic efficacy of tests for the detection of iron overload in chronic liver disease. 67 27

The relationship between the serum ferritin concentration and total body iron stores was investigated in 41 patients with idiopathic haemochromatosis and 199 first or second degree relatives. Thirty-two relatives (16.1%) had increased iron stores and serum ferritin levels were increased in all but one of them. The false-positive rate in the relatives with normal iron stores was 1.8% compared with 10% for the serum iron concentration and 33% for the transferrin saturation. There was a significant correlation between the serum ferritin concentration and both the chelatable body iron and the hepatic iron concentration. We conclude that in the natural history of classical idiopathic haemochromatosis the serum ferritin concentration is usually raised when hepatic iron stores are increased and before there is architectural damage to the liver.
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PMID:Relationship between serum ferritin and total body iron stores in idiopathic haemochromatosis. 68 May 87

1. A state of protein deficiency has been produced in rats by feeding a low protein diet, thereafter a period of rehabilitation with a normal protein but a low iron supply followed. 2. For characterization of the iron metabolism during both periods haemoglobin, total iron binding capacity, liver non-haemin iron, intestinal iron absorption and the uptake of 59Fe in the liver was determined. 3. Under these conditions the amount of 59Fe incorporated into the mucosal transferrin and the ferritin fractions has been measured. Both fractions were obtained from the supernatant of a mucosal homogenate after chromatography on sepharose 6B. 4. In anemia due to protein deficiency the typical increase of 59Fe incorporation into the fraction of mucosal transferrin--usually occuring in iron deficiency--could not be observed. This coincides with the absence of an increased iron absorption. Moreover a decrease of iron absorption is observed, which is associated with a decreased 59Fe ratio of transferrin/ferritin-fraction. 5. After normalization of the protein supply the ratio of 59Fe incorporated into the mucosal transferrin and ferritin fractions was changed remarkably in favor to transferrin together with a several fold increase of the intestinal iron absorption. 6. The conclusion is drawn that mucosal transferrin and ferritin enable the body not only to adapt the absorption to a higher but also to a lower requirement as it is the case in protein deficiency.
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PMID:The role of mucosal iron binding proteins in adaptation of iron absorption during protein deficiency and rehabilitation. 68 93

The control of hepatic iron uptake was studied in the perfused liver isolated from rats subjected to nutritional iron deficiency. The total hepatic iron uptake and incorporation into ferritin was found to be higher in iron deficiency and during the 48 h of oral refeeding with iron than in the normal state. Specific incorporation of iron into feritin from a perfusate of normal transferrin iron saturation was enhanced in nutritional iron deficiency as compared to controls after 5 h of perfusion but not after 1 h, suggesting that increased uptake of iron from the perfusate may play a role in stimulating hepatic ferritin synthesis and assembly. This promotion of uptake into ferritin was inhibited by cycloheximide suggesting that enhanced incorporation of iron is dependent upon de novo synthesis of apoferritin. In control, nutritionally iron deficient and iron-refed rats there was a significant, direct correlation between the transferrin-iron saturation of the perfusate at physiological transferrin concentrations and total hepatic iron uptake after 5 h perfusion. A significant positive correlation was found between the hepatic total and ferritin iron uptake and the transferrin synthetic rate measured in the same liver. It is proposed that in the liver the negative feedback of iron supply on transferrin synthesis may be linked with a positive feedback on ferritin synthesis. The time-course of these reciprocal responses suggests a role for hepatic ferritin and/or a component of the non-haem, non-ferritin iron pool in the regulation of transferrin synthesis.
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PMID:The control of hepatic iron uptake: correlation with transferring synthesis. 69 24


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