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

In isolated perfused rat lungs we have examined the effect of inhibition of receptor-mediated endocytosis and of intracellular acidic compartments activity on adsorptive and fluid-phase uptake and transport of macromolecules by capillary endothelium. Cationized and native ferritin were used as electron-dense tracers of adsorptive and fluid-phase transport, respectively. Luminal endothelial vesicles were labeled with tracers at 4 degrees C for 2 minutes and the density of ferritin particles in endothelial multivesicular bodies and in the capillary basement membrane, after a 60-minute chase with tracer-free perfusate at 37 degrees C, was determined by electron microscopic morphometry. Fluid-phase transport of native ferritin in 60-minute perfusions at 37 degrees C was also investigated. Adsorptive endocytosis was inhibited in chase experiments with hypertonic (800 mOsm) perfusate. Endothelial acidic compartments activity was decreased by adding either dextran sulfate or chloroquine to the chase media. We found that hypertonic solutions, dextran sulfate, and chloroquine inhibit cationized ferritin accumulation in multivesicular bodies and in the extravascular space. Hypertonic buffer or dextran sulfate have no effect on native ferritin uptake and transport in either pulse-chase or continuous perfusions. Since adsorptive or receptor-mediated mechanisms play a role in the transendothelial movement of plasma proteins, and other plasma constituents, our findings suggest a general role of the endothelial acidic compartments in modulating microvascular permeability to macromolecules.
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PMID:Inhibition of adsorptive endocytosis and transcytosis in pulmonary microvessels. 246 Jun 97

A large proportion of the milk consumed by infants in Chile is distributed by a National Food Supplementary Program. Efforts to prevent iron deficiency by milk fortification started several years ago. Initially a field study involving the simple addition of ferrous sulfate to a low-fat powdered milk was only partially successful due to the relatively low iron absorption from this product. Following the observation that the enrichment of milk with ascorbic acid markedly improved iron bioavailability, a new fortified formula was developed and has been tested in the field since 1976. This is powdered full-fat milk, biologically acidified and fortified with 15 mg Fe, as ferrous sulfate, and 100 mg ascorbic acid per 100 g powder. In a pilot study, 276 infants spontaneously weaned before 3 months of age received the fortified milk, and 278 infants receiving unfortified milk served as controls. At the end of the study (15 months of age) anemia (Hb less than 11 g/dl) was present in 25.7% of unfortified infants compared with only 2.5% in those fortified. Saturation of Transferrin less than 9% was present in 33.8% and serum ferritin less than 10 micrograms/l in 39.1% of the nonfortified infants. The figures for the fortified group were 7% and 8.5% respectively. Acceptance of the fortified formula was good. Following these observations, and as a previous step to the use of the fortified milk in the national program, the formula was tested in 7 National Health Service inner city community clinics under regular milk distribution.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevention of iron deficiency by milk fortification. The Chilean experience. 248 78

The behaviour of sideremia has been studied in order to assess the intestinal absorption of iron of a new compound, ferric chondroitin sulfate after oral administration in 12 normal volunteers. After administration of 90 mg of iron as ferric chondroitin sulfate, sideremia rose from a basal value of 88 +/- 27 micrograms/dl to a value of 128 +/- 22 micrograms/dl at the third hour. Variance analysis showed that the increases were statistically significant (F = 27.7; p less than 0.00001). In the same subjects, the test was carried out in accordance with a randomised crossover design in two periods after administration of 91 mg of ferritin iron: sideremia rose from a basal value of 92 +/- 27 micrograms/dl to a value at the third hour of 97 +/- 28 micrograms/dl, moderate increases but statistically significant (F = 3.2; P = 0.0354). Variance analysis by repeated measurements showed that increases in sideremia were significantly higher after iron administration as ferric chondroitin sulfate than after administration of ferritin iron (F = 13.18; p = 0.0042). This study documents the good bioavailability of the iron contained in ferric chondroitin sulfate.
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PMID:[Evaluation of the intestinal absorption of iron orally administered as chondroitin sulfate in normal subjects]. 250 14

Soluble and insoluble forms of ferritins have been purified from dry pea seeds by gel filtration. The insoluble form is called phytosiderin by analogy with animal hemosiderin. Native gel electrophoresis of these two forms have shown that the soluble one (ferritin) is homogenous in size and more compact than the insoluble one (phytosiderin) which is heterogenous in size. However, when iron is removed from these two classes of molecules (apoferritin), they have the same mobility in isopycnic centrifugations. Polyacrylamide-sodium dodecyl sulfate gel electrophoresis revealed a difference in their subunit composition: ferritin molecules are built up from a 28-kDa subunit and phytosiderin from a 26.5-kDa subunit. Partial proteolysis using a Staphylococcus aureus protease indicates a strong relationship between these two polypeptides. Intermediates between these two forms have also been characterized and are composed of both subunits in various amounts. Ferritin and phytosiderin are both able to incorporate iron in vitro into their mineral core. It is also shown that in vitro iron exchange induces ferritin degradation. This degradation is prevented by inhibitors of the Fenton cycle (iron chelates like o-phenanthroline and desferrioxamine B) and reduced by Tris, a radical scavenger. Under in vitro conditions of controlled radical damage the 28-kDa subunit is converted into the 26.5-kDa subunit. Purification of the 28-kDa subunit has allowed us to determine the NH2-terminal sequence. The NH2 extremity of the 26.5-kDa subunit is heterogenous, but the sequence of its main component is identical to the sequence of the 28-kDa subunit downstream residue Leu-21. These data indicate that the 26.5-kDa subunit is produced by radical mediated damage leading to a series of cleavages in the NH2 terminal part of the 28-kDa subunit.
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PMID:Mechanism of the transition from plant ferritin to phytosiderin. 253 54

The synthesis of ferritin is regulated at the translation level in coordination with iron availability. Under conditions of low iron, translation of ferritin mRNA is repressed and the majority of ferritin mRNA is non-polysomal. Upon an increase in iron, translation of ferritin mRNA is derepressed resulting in as much as a 50-100-fold increase in the rate of ferritin synthesis. This regulation is mediated at least in part by a specific translational repressor which binds to a conserved sequence, the iron responsive element, located in the 5'-untranslated region of ferritin mRNA. In this communication we report the purification of such a repressor from rabbit liver. This repressor, which we call the "ferritin repressor protein," has an apparent molecular mass of 90 kDa when analyzed by gel filtration chromatography. It inhibits translation of ferritin mRNA in a highly specific fashion when added to a wheat germ lysate programmed with liver poly(A+) mRNA. In addition, it binds specifically to sequences contained within the first 92 nucleotides of ferritin mRNA, most likely the iron responsive element. Analysis of highly purified repressor by sodium dodecyl sulfate-polyacrylamide gel electrophoresis shows that it is composed primarily of a single polypeptide of approximately 90 kDa. Elution of this 90-kDa polypeptide from a sodium dodecyl sulfate gel followed by renaturation and analysis for repressor activity shows that it both binds to the 5'-untranslated region of ferritin mRNA and represses its translation in vitro.
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PMID:Purification of a specific repressor of ferritin mRNA translation from rabbit liver. 256 64

To study components of anionic sites on the lamina densa of the dermo-epidermal junction (DEJ) and to assess the effect of removal of sialic acid or glycosaminoglycans on its charge-selective permeability, epidermal sheets, whose dermis had been removed by treatment with dithiothreitol, were digested with heparitinase, chondroitinase ABC, hyaluronidase, or neuraminidase. They were then stained with polyethyleneimine for demonstration of the anionic sites or incubated in a medium containing native anionic ferritin for tracer experiments. The anionic sites were completely removed after heparitinase digestion. Although the numerical density of the sites was not altered, their electron density was decreased after chondroitinase ABC digestion. The other enzymes had no effect on the sites. In the tracer experiments, heparitinase or neuraminidase increased the number of tracer molecules penetrating into the lamina lucida of the epidermal sheet, while the other enzymes had no effect on it. These data indicate that heparan sulfate, which is a main component of the anionic sites, plays an important role in the charge-selective permeability of the DEJ, whereas chondroitin sulfate, which seems to be contained in the sites, does not, probably because of its small amount. These data also indicate that sialic acid, which is not a main component of the anionic sites demonstrated with the cationic probe, has a role in the permeability function.
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PMID:Effect of enzyme digestion on anionic sites and charge-selective permeability of dermo-epidermal junction. 258 48

Iron deficiency may develop in prolonged breast feeding. Introduction of beikost (supplementary nutrition) is recommended in Germany for infants after 4 months of age. In a prospective study 73 exclusively breastfed infants at the age of 16 weeks were assigned to one of two feeding groups: 35 infants received a meat vegetable dinner fortified with iron-2-sulfate (3 mg iron per 100 kcal) as their first supplementary food. At 20 weeks of age a milk based rice cereal (MBRC) without iron fortification was added as a second beikost meal. The other group comprised 38 infants who first received a MBRC fortified with iron-3-pyrophosphate (3 mg iron per 100 kcal). At 20 weeks of age a non iron fortified vegetable potato dinner was introduced. After 6 months of age the iron fortified meat vegetable dinner was offered to all infants once a day. 26 infants who did not receive this dinner but otherwise were consulted and treated identically served as controls at 12 months of age. At 6 months of age values of hemoglobin, MCV, serum iron, ferritin, and transferrin saturation were higher in the meat dinner group compared to the cereal first group. At 12 months of age this was also true for the meat dinner group compared to the controls. However, the differences were minor and statistically not significant. Whereas most of the indicators of iron nutritional status were within the lower normal range, and total iron intake was below the levels recommended by German and American authorities, recommending two iron fortified beikost meals between age 7 and 12 months appears to be justified.
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PMID:[Preventing iron deficiency in breast-fed infants by suitable supplementary food. A prospective, controlled study]. 262 46

Adequate body iron stores are crucial to assuring rapid and complete response to recombinant human erythropoietin (rHuEPO). In the present study, markers of iron storage were examined in 27 patients with normochromic, normocytic anemia undergoing acute rHuEPO (150 to 300 U/kg t.i.w.) treatment for anemia. We calculated projected iron needed for new hemoglobin synthesis from the difference between initial and target hemoglobin concentrations, initial iron reserves available from initial serum ferritin levels, and net projected surplus or deficit from the difference between needs and reserves. Of 22 patients predicted to develop iron deficiency (mean projected deficit 268 +/- 70 mg), 20 developed evidence of exhausted iron stores (transferrin %sat less than 16 or ferritin less than 30 micrograms/liter) before reaching target hemoglobin; two predicted to become deficient (projected deficit less than 100 mg) did not; and all five predicted to avoid iron deficiency (mean projected surplus 177 +/- 20 mg) remained iron replete. During acute rHuEPO therapy net body iron balance remained neutral in patients receiving no iron supplements and increased 5 mg/kg in patients prescribed oral ferrous sulfate. However, in patients given iron dextran i.v. less than 60% of elemental iron administered became measurable as iron stores or usable for hemoglobin synthesis.
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PMID:Iron status in patients receiving erythropoietin for dialysis-associated anemia. 270 74

In order to reveal the pathway of iron release from macrophages, a 59Fe-labelled ferric hydroxide-potassium polyvinyl sulfate complex (Fe-PVS) was injected intravenously into anemic rats and the level of radioactivity in the liver, spleen, bone marrow, blood plasma and red blood cells (RBC) was estimated at various time intervals after the injection. Histochemical observation of ferric iron and ferritin in the liver was also made on anemic rats treated using unlabelled Fe-PVS. Fe-PVS injection promoted the recovery of anemia causing a rapid increase in the RBC number, with activated erythropoiesis occurring in the spleen and bone marrow. Soon after the injection, most of the radio iron was found in the liver with a small amount in the circulating erythrocytes, bone marrow and spleen. The iron level in the liver decreased gradually with a rapid increase in the iron level of the erythrocytes which reached a very high level 6 days after the 59Fe-PVS injection. Histochemical observations showed a heavy deposition of ferritin in the Kupffer cells 3 days after Fe-PVS injection. This deposition was minimized after 6 days with an increase in the level of ferritin in the parenchymal cells in the central area of acini. The level of radioferritin estimated biochemically in the nonparenchymal cell fractions of the liver revealed that the level dropped by about one third approximately 3.5 days after the Fe-PVS injection, showing the stimulated ferritin release at this stage. Results indicate that Kupffer cells in the liver play an important role in ferritin synthesis from the phagocytized iron compounds and that the iron is supplied for erythroid cell proliferation.
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PMID:An experimental study on the pathway of iron transfer from macrophages to erythrocytes in rat liver. 272 Jul 98

In order to examine the effects of mild iron deficiency on physical work capacity, 40 prelatent iron-deficient female endurance runners were studied before and after 8 wk of supplementation with either oral iron (320 mg ferrous sulfate) or a matching placebo. Subjects underwent the following physical work capacity tests: the Wingate cycle ergometer test, the anaerobic speed test, the ventilatory threshold, VO2max, and maximal treadmill velocity during the VO2max test. Muscle biopsy samples pre- and post-treatment were obtained from 17 of the subjects, and these were assayed for citrate synthase and cytoplasmic alpha-glycerophosphate dehydrogenase activity. Subjects were randomly assigned to one of the treatment groups, and a double-blind method of administration of the supplements was used. The differences in improvement scores between the two groups on the work capacity and enzyme activity variables were statistically nonsignificant (P greater than 0.05). Serum ferritin values rose from a mean of 12.4 +/- 4.5 to 37.7 +/- 19.7 ng.ml-1 for the experimental group and from 12.2 +/- 4.3 to 17.2 +/- 8.9 ng.ml-1 for the controls (P = 0.0025), whereas hemoglobin levels remained fairly constant for both groups (P = 0.6). Eight weeks of iron supplementation to prelatent/latent iron-deficient, physically active females did not significantly enhance work capacity. Within the limitations of this study, the presence of a serum ferritin below 20 ng.ml-1 does not pose a significant handicap to physical work capacity.
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PMID:The effects of prelatent/latent iron deficiency on physical work capacity. 273 74


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