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

A number of iron chelating agents, consisting largely of hydroxamic acid and benzoic acid derivatives, have been studied in an in vitro Chang cell culture system to determine their effect on cellular iron uptake, ferritin synthesis and the incorporation of iron into ferritin. The results have been compared with those of a previous study in which iron balance was determined in hypertransfused rats. Both techniques appear to be of value in screening new iron chelating agents for potential therapeutic use in patients with iron overload.
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PMID:The use of chang cells cultured in vitro to evaluate potential iron chelating drugs. 100 21

The disruption of lysosomes with release of their content of lytic enzymes was an early concept for the possible role of these organelles in the pathogenesis of tissue damage. Many examples are known of primary lysosomal storage diseases due to a congenital deficiency of certain acid hydrolases. It is suggested that iron overload due to either primary haemochromatosis or transfusional siderosis is a form of acquired secondary lysosomal storage disease. Subcellular fractionation experiments and electron microscopic studies have shown that liver tissue from patients with iron overload has iron-laden lysosomes. Similar results have been found in iron-overloaded rats. In patients, but not in experimental animals, enzymic analyses have shown increased activities of acid hydrolases and strikingly enhanced lysosomal fragility in liver homogenates. When it has been possible to deplete the patients of the excessive iron, these parameters have returned to normal. The possible mechanisms by which the iron compounds disrupt lysosomes, including distension with ferritin or haemosiderin or free-radical-mediated membrane damage, will be discussed.
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PMID:Lysosomal disruption in the pathogenesis of hepatic damage in primary and secondary haemochromatosis. 105 36

During a study of pathogenetic mechanisms in the hepatic cirrhosis of thalassaemia major, 16 liver biopsies were examined by electron microscopy. Previous ultrastructural studies of liver cells during iron overload have shown electron-dense iron as lysosomal haemosiderin, and as lysosomal and cell-sap ferritin. In this study, all biopsies, regardless of the patient's age, showed ferritin molecules within lysosomes in a specific pattern in relationship with regularly arranged lamellae. This membrane-associated lysosomal ferritin is considered to be a stage in the segregation of iron seen in iron overload. The dimensions and electron density of individual ferritin molecules indicate differences between cell sap and lysosomal ferritin. Intracellular ferritin transport and iron-seclusion mechanisms are reconsidered in view of these findings. The liver biopsies of thalassaemic infants also provide information about the causal relationship between iron overload and collagen deposition. Since the collagen deposition precedes any morphological evidence of cellular injury (other than the increased iron content), the primary cirrhotogenic factor in thalassaemia is apparently not cell necrosis but possibly excessive collagen deposition induced by iron.
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PMID:The liver in thalassaemia major: ultrastructural observations. 105 35

An immunoradiometric assay was used to determine serum ferritin in patients with iron overload disorders and in patients with liver disease. In patients with iron overload, serum ferritin was closely correlated in an exponential manner with quantitative measurements of storage iron; however, a different relationship applied when storage iron levels were within normal range, suggesting that circulating ferritin is in equilibrium with two functionally distinct tissue ferritin pools. High ferritin levels were common in patients both with acute and chronic liver disease, normal values being virtually confined to women and to subjects with a history of recent hemorrhage. In liver disease generally, serum ferritin varied both with the serum transaminase level and with liver iron concentration, but correlated well with neither factor separately. There was no correlation with the serum iron or total iron-binding capacity. An extremely close correlation was found between serum ferritin and an empirical index derived from the product of the serum transaminase times liver iron concentration, implying that the circulating level depended on both the degree of hepatocellular injury and liver iron store. There was a close linear correlation between the serum ferritin-transaminase ratio and liver iron concentration in all disorders studied, and this index may prove to be the most useful value for diagnostic purposes.
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PMID:Serum ferritin in patients with iron overload and with acute and chronic liver diseases. 111 54

The ferritin concentration of the formed elements of the blood has been measured. Nearly equal amounts were found in plasma, red cells, granulocytes, and in the mononuclear (monocyte and lymphocyte) cell fraction. Platelets contained a negligible amount. Concentrations of ferritin were greatest in blood leukocytes, amounting to approximately 24 mug/ml. Changes occurring with iron depletion and iron overload were consistent with those expected in body tissues in general. With infection, increased levels of ferritin were observed in the mononuclear cell fraction, consistent with that which occurs in RE cells.
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PMID:Ferritin in formed blood elements (38539). 112 82

Serum ferritin concentration was measured by immunoradiometric assay in 64 subjects. It was closely related to the size of body iron stores measured by hemosiderin content of bone marrow in all subjects and by the deferoxamine test in 10 patients with iron overload. Urinary cobalt excretion, an indirect measure of iron absorption, was inversely related to hemosiderin content of bone marrow in 34 patients aged 18 to 72 with or without liver disease, but this relation did not hold in a group of 20 student volunteers aged 17 to 30, indicating that the test is unreliable in young people. A strong inverse correlation was demonstrated between values for cobalt excretion and serum ferritin in the 34 patients and between those for iron absorption and serum ferritin in the 20 students. Serum ferritin concentration appears to reflect accurately the iron status of the healthy individual but high values in liver disease must be interpreted with caution.
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PMID:Serum ferritin, cobalt excretion and body iron status. 112 86

1. The properties of ferritin in serum have been compared with those of ferritin from a number of tissues including blood cells. On anion-exchange chromatography with DEAE-Sephadex, the behaviour of human heart ferritin is different from that of liver, kidney or spleen ferritin. Reticulocyte ferritin appears to have similar characteristics to heart ferritin. 2. Serum ferritin from normal subjects and patients with various degrees of iron load, leukaemia or liver disease all have a much lower affinity for the anion-exchange column that any tissue ferritin, suggesting a difference in isoelectric point. The elution point of serum ferritin from patients with acute myeloblastic leukaemia is significantly different from normal. 3. Density gradient centrifugation in sucrose showed that ferritin in leucocyte extracts and partially purified ferritin from the serum of two patients with iron overload behaved as apoferritin rather than the iron-rich protein. 4. The results suggest that ferritin is modified during its entry into the plasma and that even in cases of iron overload the iron content of serum ferritin may be low. The findings are of importance in considering the origin of plasma ferritin, the clearance of ferritin from plasma and its role in iron metabolism.
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PMID:The characteristics of ferritin from human tissues, serum and blood cells. 116 59

Purified tissue ferritins isolated from Bantu subjects with gross haemosiderosis, from a patient with idiopathic haemochromatosis (HC) treated by phlebotomy, and from rats with experimental iron overload were studied in order to determine the significance of the abnormality previously demonstrated in tissue isoferritins in patients with IHC. The isoferrin profile of the tissues from the Bantu subjects and the iron-loaded rats showed a similar abnormality to that previously found in patients with untreated IHC--that is, an abnormally uniform distribution of iron-containing isoferritins with an increase in the more basic isoferritins and an apparent absence of the more acidic ones. In contrast, tissues from the patient with treated IHC, who was iron depleted at the time of death, showed the normal organ-specific isoferritin distribution. These findings strongly suggest that the abnormal distribution of tissue isoferritins in IHC is an acquired phenomenon and unlikely to be related to an underlying genetic defect in ferritin or iron metabolism.
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PMID:Alterations in tissue ferritins in iron storage disorders. 119 19

A sensitive, specific and precise immunoradiometric assay for ferritin has been developed. Ferritin was measured in the serum of 160 hospital controls, 101 females (118 +/- 9 mug/l) and 59 males (189 +/- 16 mug/l). This difference was statistically significant. In 28 patients with untreated iron deficiency anaemia, serum ferritin concentration (6.1 +/- 0.7 mug/l) was significantly lower than in the controls, but it was within the normal range in 14 cases of polycythaemia vera treated by repeated phlebotomy. In 4 patients with primary haemachromatosis (2884 +/- 56 mug/l), 25 with secondary iron overload states (5702 +/- 1235 mug/l) and 8 with haemolytic anaemia (1612 +/- 605 mug/l), serum ferritin levels were markedly elevated. In 14 cases of transfusional siderosis there was a highly significant correlation between serum ferritin concentration and units of blood transfused. A circadian rhythm in serum ferritin concentration was observed in 7 healthy subjects.
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PMID:Immunoradiometric assay for ferritin in human serum. 121 36

Iron deficiency is one of the most serious nutritional problems confronting the United States and the world today. An understanding of the mechanisms operative in the control of uptake and utilization of iron is essential to develop suitable prophylactic and therapeutic strategies. Iron excess can also be a serious health hazard. Studies on Bantu siderosis, hemochromatosis and other overload pathologies also provide insight into the intake and storage of this metal. Several models for iron transport across the mucosal membrane are developed. The most satisfactory seems to involve chelation of the iron to provide solubility diffusion passively across the gut membrane, and equilibrium binding to various storage sites within the tissue. Both ferric and ferrous forms are available. The solution chemistry of iron governs its biological behavior. Low-molecular-weight compounds present in normal dietary foodstuffs, as well as those prepared synthetically, can enhance the uptake of oral iron. Suitable application of complexes of iron with fructose, nitrilotriacetate, citrate and other molecules should be efficacious in the treatment of iron deficiency anemia. Potential dangers of food fortification with iron are acknowledged, and application of immunoassay techniques for measuring circulating ferritin suggest it as a rapid and inexpensive monitor for overload.
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PMID:Tired blood and rusty livers. 125 66


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