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

In the present paper we apply the "ecotaxis hypothesis" to the analysis of lymphocyte distribution in Hodgkin's disease and other forms of lymphoid malignancy. The results lead us to consider the possiblity that metal-binding proteins, namely ferritin, transferrin and lactoferrin, play a role in lymphocyte ecotaxopahty. It is suggested that in Hodgkin's disease, a failure of lymph node and spleen monocytes to handle iron normally could explain most of the hematologic, immunologic, pathologic, and epidemiologic features of the disease.
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PMID:Suggested models of ecotaxopathy in lymphoreticular malignancy. A role for iron-binding proteins in the control of lymphoid cell migration. 30 76

The circulating red blood cells formed in bullfrog larvae, chicken embryos, and mouse embryos contain large amounts of ferritin and storage iron in excess of the need for hemoglobin. In contrast, the circulating red cells of adult animals contain little ferritin. Ferritin synthesis and iron storage are coordinated with differentiation and hemoglobin synthesis in the red cells of adults. In order to test the hypothesis that ferritin synthesis could be controlled independently of hemoglobin synthesis and differentiation in the red cells formed early in life, bullfrog larvae were injected with iron to determine if ferritin synthesis was increased in the circulating red cells. Within 17 h after the injection of iron, the synthesis of ferritin, assayed as the incorporation of [14C]leucine by cell suspensions prepared from circulating red cells, was increased from 2.9 to 10.2% of the total protein, and the specific activity of the ferritin synthesized increased from 1100 to 3000 cpm/A280. There was no change in the hematocrit of the animals nor in the specific activity of hemoglobin synthesized by suspensions of red cells (average, 720 cpm/A280). The results suggest that in mature, larval red cells, ferritin synthesis can be controlled by changes in the extracellular environment. The results also indicate that ferritin synthesis can be controlled independently of hemoglobin synthesis with which it is coordinated during erythroid differentiation in adult animals.
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PMID:The induction of ferritin synthesis in circulating larval red blood cells. 30 18

A prospective study was performed over 15 months to determine the cause of iron deficiency in adult males and postmenopausal females attending a general hospital. The laboratory computer identified all subjects with a haemoglobin less than 10.6 g/dl and a mean corpuscular volume less than 86 fl. Patients becoming anaemic after trauma or recent surgery were excluded. The iron status of each patient was assessed by serum iron studies, serum ferritin or sternal marrow aspiration. Reduced red cell indices and blood film morphology were not diagnostic of iron deficiency. Of 215 patients assessed, about half (103) were found to be iron replete. This group had a variety of disorders--malignancy, chronic inflammation, chronic renal and non-malignant haematological diseases. The other group of 104 patients satisfied criteria for iron deficiency, and 100 of these were investigated further. The cause of iron deficiency was found in all but three subjects. Inadequate dietary intake was a contributing factor in over half of the patients and 40 regularly took salicylates. Investigation defined a source of chronic gastrointestinal blood loss in most instances.
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PMID:Iron deficiency anaemia--a prospective study. 31 71

An immunoperoxidase staining technique was used for detecting three major iron-binding proteins (transferrin, ferritin, and lactoferrin) in routine histological paraffin sections of human tissue. Transferrin was found mainly in hepatocytes, a variety of epithelial and myoepithelial cells, renal tubular cells, and histiocytes. Ferritin was most readily found in histiocytes and liver cells, with weaker reactions seen in epithelial cells. Lactoferrin was found in lactating breast tissue, bronchial glands, polymorphs, and gastric and duodenal epithelial cells. The technique is potentially valuable for investigating abnormal iron states.
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PMID:Distribution of transferrin, ferritin, and lactoferrin in human tissues. 34 12

87 patients with end-stage renal failure on long-term hemodialysis, 25 not on dialysis and 37 with renal transplants have been studied. Serum ferritin was measured by immunoradiometric and radioimmuno-assay. The correlation between the two methods was excellent (p less than 0.001). In 25 patients on long-term hemodialysis a good correlation was found between serum ferritin levels and stainable iron (p less than 0.001). All patients with adequate iron stores had serum ferritin levels above 60 ng/ml, whereas only one out of 10 with decreased or absent iron stores had a higher leve (118 ng/ml). According to these criteria the iron stores were decreased in 59% of our patients on long-term hemodialysis, decreased or adequate in 14% and adequate or increased in 27%. There was no correlation between serum ferritin levels and serum iron and total iron binding capacity. The distribution pattern of the serum ferritin levels was log normal and did not significantly differ in the three groups studied, although the patients with renal transplants had nearly normal hemoglobin and creatinine levels. Elevated serum ferritin levels in patients (21%) on hemodialysis could only partly be explained by repeated transfusions or chronic infections.
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PMID:[Serum ferritin in renal insufficiency, hemodialysis and kidney transplantation]. 36 27

The effect of endotoxin on the processing of erythrocyte iron by reticuloendothelial cells of the liver and spleen was studied in rats using heat damaged erythrocytes labelled with 59Fe. Endotoxin did not alter the uptake of the damaged cells but markedly inhibited the subsequent early phase of iron release from the reticuloendothelial cells. The inhibition seemed to be due to both a decreased rate of labelled haem destruction and an increased incorporation of radioiron into ferritin. Although early iron release was decreased 0--2 h after endotoxin administration, the diversion of iron into ferritin was more marked when endotoxin was given 18 h before. The block in iron release was partially overcome in animals that had been kept on an iron free diet or had been phlebotomised. In these animals the decreased rate of haem catabolism remained unaltered but less iron was diverted into ferritin.
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PMID:The mechanism of endotoxin-induced hypoferraemia. 36 29

A year-long double-blind study of 2,3-dihydroxybenzoic acid (2,3-DHB) given orally at a dose of 25 mg/kg four times per day was undertaken in 15 patients with beta-thalassemia major. 2,3-DHB and placebo (mannitol) were tolerated to an equal degree and there were no signs of drug toxicity at the end of 1 year. Efficacy in terms of retardation of iron accumulation could be documented using serial liver biopsies, serum ferritin determinations, or clinical laboratory assessment. Serum iron values increased, as did the iron binding capacity, in the group receiving 2,3-DHB. The increase in iron binding capacity was due to drug interference with the method of determination. Because of the greater efficacy of slow infusions of desferrioxamine in chelating iron when administered slowly, the clinic has shifted its emphasis toward further evaluation of that compound. Nevertheless, in view of the minimal toxicity of 2,3-DHB, further work appears warranted to define its role in the treatment of iron-overload.
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PMID:Chelation therapy in beta-thalassemia major: a one-year double blind study of 2,3-dihydroxybenzoic acid. 37 74

Over the last few years the study of idiopathic haemochromatosis has not brought to light any basic change in the overall pattern of organic and metabolic damage produced by the disease and comprising altered skin pigmentation, liver disease, diabete mellitus, heart disease, endocrine dysfunction, bone and joint disease. Nevertheless, certain facets of the clinical picture have been described and progress has been made in understanding the signs of the disease. Although the desferrioxamine test is no without merit, especially if performed after vitamin C administration, for measuring the extent of iron overload, two methods seem better equipped: serum ferritin radioimmunoassay and measurement of iron concentration in a liver biopsy specimen. The HLA antigen A3 and, more especially, haplotype A3, B14, are markers for the genetic basis of the disease. Repeated phlebotomy therapy generally brings about symptomatic improvement and a significant increase in survival.
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PMID:[Idiopathic haemochromatosis. I. Clinical, biological and therapeutic aspects (author's transl)]. 37 16

(1) Brief introduction to iron metabolism and the biochemistry of ferritin. (2) Early studies of circulating ferritin. (3) Methods for measuring serum ferritin concentrations -- immunoradiometric, radioimmuno- and enzyme-linked immuno assays based on liver or spleen ferritin -- an evaluation of these techniques. (4) Serum ferritin concentrations in normal subjects -- definition of normality -- relationship between storage iron and serum ferritin concentrations -- changes during development from birth to old age -- iron deficiency -- variability of serum ferritin concentration -- evaluation of use of ferritin assay for assessment of storage iron levels. (5) Serum ferritin concentrations in disease -- hemochromatosis -- secondary iron overload -- liver damage -- infection and chronic disease -- cancer. (6) Assay of serum ferritin with antibodies to ferritins other than liver or spleen -- ferritinemia and cancer. (7) Properties of serum ferritin -- molecular weight -- iron content -- isoelectric focusing patterns -- carbohydrate content -- immunological properties. (8) Physiology of circulating ferritin -- release of ferritin from tissues -- origin of circulating ferritin -- clearance from the plasma -- iron and protein turnover. (9) Summary -- factors influencing serum ferritin concentrations and clinical use of ferritin estimations.
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PMID:Serum ferritin. 37 39

Seventy-three patients with several haematological diseases have been studied with radio-iron-kinetic, cyto-chemical measurement of iron in the bone marrow, and radio-immunometric determination of the ferritin in the serum. This method gives results which correlate significantly with other methods which evaluate the iron storage pool, in normal or iron-deficient patients. In some cases, an excess of serum ferritin, contrasting with normal serum iron, is confirmed by cytochemical and/or Fe-kinetic studies. In myeloproliferative diseases however, secretion of ferritin by immature cells may induce an excess of serum ferritin. In such cases, the dosage of ferritinaemia cannot be considered as an index of the iron storage pool. Future development of specific dosage of isoferritins could enable to measure the true iron stores, as well as to give an index estimating the evolution of the abnormal cell population.
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PMID:[Radio-immunometric determination of the ferritin for evaluation of the iron storage pool (author's transl)]. 37 12


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