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

We undertook studies in the isolated perfused rat lung to determine 1) the effects of endothelial charge neutralization with the polycation protamine sulfate on microvascular permeability, lung water, and anionic ferritin binding to the endothelium and 2) the role of heparan sulfate and hyaluronate, negatively charged cell surface glycosaminoglycans, on permeability. Capillary permeability was determined by tissue 125I-albumin accumulation in isolated perfused rat lungs. In control lungs the 5-min albumin uptake was 0.50 +/- 0.05 cm3.s-1.g dry tissue-1 X 10(-3). It was increased by 132 +/- 7.8% (P less than 0.001) by protamine (0.08 mg/ml) and 65 +/- 12% (P less than 0.01) by heparinase (5 U/ml), whereas hyaluronidase (25 NFU/ml) was without effect. In control lungs total water was 4.83 +/- 0.15 ml g/dry tissue. Protamine increased lung water 12 +/- 2% (P less than 0.05). Heparinase caused a 9 +/- 3% increase (P less than 0.05), and hyaluronidase had no effect. Electron microscopy demonstrated that protamine increased anionic ferritin binding to the surface of endothelial cells. We conclude that protamine sulfate neutralization of negative charge in the pulmonary microcirculation leads to increased microvascular permeability. Heparin sulfate may be responsible for this charge effect.
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PMID:Effects of protamine, heparinase, and hyaluronidase on endothelial permeability and surface charge. 369 32

Milk replacers containing 100, 500, 1000, 2000, or 5000 ppm iron were fed to 3-d-old calves for 6 wk to estimate the lowest amount of dietary iron (added as ferrous sulfate) that would reduce calf performance. Calves tolerated all iron treatments except 5000 ppm. At this intake calves showed reduced weight gains, DM intake, feed efficiency, and digestibility of DM and protein. There were no other signs of iron toxicity and no gross abnormalities were found on postmortem examination. Percent of dietary iron in feces increased with higher dietary iron and ranged from 65 to 84%. Elevated iron intakes caused relatively small increases in iron concentration of blood plasma, bile, kidney, heart, and muscle but marked increased in spleen and liver iron, particularly in liver for the 2000 and 5000 ppm treatments. At 100 ppm iron intake, nonheme iron in liver, spleen, and kidney was composed of similar proportions of ferritin and hemosiderin, but at 5000 ppm iron intake, hemosiderin predominated in these tissues. Thus, the preruminant calf tolerated between 2000 and 5000 ppm iron in milk replacer. At toxic iron intake, calf performance and feed efficiency were reduced; there was a characteristic change to higher liver than spleen iron; and hemosiderin became the predominant iron storage compound in both tissues.
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PMID:Effect of excess iron in milk replacer on calf performance. 369 37

Radioiron was introduced into the intestinal lumen to evaluate absorption, injected as nonviable red cells to evaluate reticuloendothelial (RE) processing of iron, and injected as hemoglobin to evaluate hepatocyte iron processing. Redistribution of iron through the plasma was evaluated in control animals and animals whose transferrin was saturated by iron infusion. Radioiron introduced into the lumen of the gut as ferrous sulfate and as transferrin-bound iron was absorbed about half as well in iron-infused animals, and absorbed iron was localized in the liver. The similar absorption of transferrin-bound iron suggested that absorption of ferrous iron occurred via the mucosal cell and did not enter by diffusion. The decrease in absorption was associated with an increase in mucosal iron and ferritin content produced by the iron infusion. An inverse relationship (r = -0.895) was shown between mucosal ferritin iron and absorption. When iron was injected as nonviable red cells, it was deposited predominantly in reticuloendothelial cells of the spleen. Return of this radioiron to the plasma was only 6% of that in control animals. While there was some movement of iron from spleen to liver, this could be accounted for by intravascular hemolysis. Injected hemoglobin tagged with radioiron was for the most part taken up and held by the liver. Some 13% initially localized in the marrow in iron-infused animals was shown to be storage iron unavailable for hemoglobin synthesis. These studies demonstrate the hepatic trapping of absorbed iron and the inability of either RE cell or hepatocyte to release iron in the transferrin-saturated animal.
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PMID:The effect of transferrin saturation on internal iron exchange. 374 34

Soy products have been reported to inhibit absorption of nonheme food iron and fortification iron. Iron bioavailability from a soy formula (Prosobee-PP 710) (iron added as ferrous sulfate: 12 mg/L; ascorbic acid: 54 mg/L) was examined in 16 adult women using the extrinsic radioactive tag method. The geometric mean absorption from the soy formula was only 1.7%. The effect of this formula on iron nutrition in infants was studied in 47 healthy term infants weaned spontaneously before 2 months of age and who received the formula ad libitum until 9 months of age. For control, 45 infants received a cow's milk formula fortified with ferrous sulfate (iron: 15 mg/L; ascorbic acid: 100 mg/L), which has been shown to be effective in preventing iron deficiency, and 49 additional breast-fed infants were also followed. All babies received solid foods (vegetables and meat) starting at 4 months of age. Iron nutritional status was determined at 9 months. Infants fed soy formula and iron-fortified cow's milk had similar mean values of hemoglobin, mean corpuscular volume, transferrin saturation, free erythrocyte protoporphyrin, and serum ferritin; both formula groups differed significantly (P less than .05) from the breast-fed group in all measurements except free erythrocyte protoporphyrin. Anemia (hemoglobin less than 11 g/dL) was present in only 4.3% and 2.2% of infants receiving the soy and the fortified formulas, respectively, v 27.3% in the breast-fed group. These results indicate that soy formula, in spite of the lower iron bioavailability when measured in adults, is essentially as effective as iron-fortified cow's milk in preventing iron deficiency in infants.
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PMID:Bioavailability of iron in soy-based formula and its effect on iron nutriture in infancy. 376 74

Phagocytosis and bactericidal capacity of neutrophils were measured in 10 iron-deficient infants age 6-23 mo. All infants had hemoglobins less than 11 mg/dL with low saturation of transferrin and serum ferritin but were otherwise in good health. Neutrophil function and iron status were assessed at 0, 3-5, 15, 30, and 90 days of oral iron therapy. Phagocytosis was unaffected in iron deficiency and remained unchanged during therapy. Bactericidal capacity was severely impaired prior to treatment. After 3-5 days of ferrous sulfate administration, there was no significant improvement. At day 15 it returned to normal ranges and remained so at days 30 and 90. The sequence of events suggests that iron does not have a direct effect upon circulating neutrophils but, rather, that it is required during the development of neutrophils in the bone marrow.
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PMID:Effect of iron therapy on phagocytosis and bactericidal activity in neutrophils of iron-deficient infants. 378 34

To label heparan sulfate proteoglycans and other strong anions within glomerular basement membranes (GBM) during assembly, cationized ferritin (CF), with a narrow isoelectric range of 7.7 to 8.2, was intravenously injected into newborn rats. Kidneys were then fixed and processed for electron microscopy at intervals ranging from 1 to 72 h after CF injection. One hour after injection, CF bound extensively to the lamina rara interna and externa of developing GBM and mesangial matrix and to tubular basement membranes (TBM). In double basement membranes of early stage glomeruli, large amounts of CF were also seen in central areas between the endothelial and epithelial basement membranes. In maturing-stage glomeruli, CF bound throughout interior regions of GBM outpockets projecting into the epithelial side of capillary walls as well as to the laminae rarae. Because in adult rats CF binds only to the laminae rarae, the abundant anionic sites seen here in newborns between double basement membranes and within GBM outpocket interiors may be subsequently neutralized or removed during the GBM assembly process. In addition to basement membranes, CF was also located intracellularly within endocytic vesicles and lysosomes of glomerular endothelial, mesangial, and epithelial cells 1 h postinjection. CF was also present in similar structures within the tubular epithelium. In contrast to these findings, CF was gradually lost from developing GBM 5, 15, and 24 h after injection and was essentially cleared from all GBM, mesangial matrices, and TBM after 48 h. Large CF aggregates were progressively accumulated within mesangial lysosomes, however. The transient binding of CF to GBM anionic sites seen here was most likely due to its endocytic removal by developing glomerular endothelial, mesangial, and epithelial cells. Anions in the circulation probably also competed effectively with the GBM and TBM for bound CF.
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PMID:Distribution of intravenously injected cationized ferritin within developing glomerular basement membranes of newborn rat kidneys. 380 1

The polycation hexadimethrine (HDM) binds to anionic sites in the glomerular basement membrane (GBM) and causes heavy proteinuria when infused in vivo. An in vitro assay of 3H-HDM binding to isolated dog GBM was developed, to permit further analysis of the GBM components binding HDM. 3H-HDM binding to isolated GBM was saturable, reversible in dose-dependent fashion by competing polycations, and inhibited by increasing salt concentration and low pH. The pH dependence of binding suggested that most of the HDM binds to carboxyl groups rather than to the sulfate groups of proteoglycans. Removal of heparan sulfate by heparinase or purified heparatinase had no detectable effect on HDM binding. Treatment of GBM with neuraminidase, hyaluronidase, or chondroitinase reduced binding of HDM by a maximum of 20 to 38%. However, substitution of carboxyl anions with nonionizable glycine methyl ester residues resulted in complete elimination of HDM binding. Parallel results were obtained in studies of glomerular localization of cationized ferritin (CatF), pI 8.5. After carboxyl substitution, GBM did not bind CatF; heparinase-treated GBM bound CatF in a distribution not demonstrably different from normal. Cellulose acetate electrophoresis of glycosaminoglycan fractions prepared from treated GBM confirmed that carboxyl modification did not alter the content or charge of the heparan sulfate of GBM, but heparinase treatment removed at least 90% of heparan sulfate. The results indicate that carboxyl groups are quantitatively more important than heparan sulfate for binding of HDM in vitro. Since HDM causes proteinuria in vivo, carboxyl groups may be important for maintenance of normal permselectivity.
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PMID:Polycation binding to glomerular basement membrane. Effect of biochemical modification. 380 16

A randomized, double-blind trial of iron replacement after repeated blood donation was conducted in 75 menstruating women; 51 completed the study. Volunteers were assigned randomly to one of three treatment groups: 1) carbonyl iron (nontoxic elemental iron powder), 600 mg; 2) ferrous sulfate, 300 mg (60 mg Fe++); or 3) placebo, each given three times daily for 1 week immediately after blood donation. Blood samples obtained initially and 56 days later were tested for hemoglobin, mean corpuscular volume (MCV), free erythrocyte protoporphyrin, serum ferritin, serum iron, total iron binding capacity (TIBC), and percent saturation of TIBC. The prevalence of gastrointestinal side effects was similar in both groups taking iron. At the end of the study there was no laboratory evidence of change in iron status in women who received carbonyl iron (n = 15). In those treated with ferrous sulfate (n = 17) the mean TIBC increased (p less than 0.001), and in the placebo group (n = 19) there were decreases in mean MCV (p less than 0.01), serum ferritin (p less than 0.001), and percent saturation (p = 0.027) with an increase in mean TIBC (p = 0.004). Carbonyl iron seems to be effective for short-term iron replacement in repeat blood donors and may have the advantage of decreased or absent risk of poisoning if accidentally ingested by children.
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PMID:Carbonyl iron for short-term supplementation in female blood donors. 381 Aug 31

Emulphogene-solubilized chicken macrophages were used for the isolation of the mannose receptor by affinity chromatography on mannose-sepharose. From 5 X 10(9) cells 1 microgram protein was obtained, which was separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) into 2 bands with an approximate molecular weight of 130 and 170 kDa. The agglutinating activity was assayed with mannan-coated M. luteus cells. Agglutination was inhibited by D-mannose, L-fucose and D-N-acetylglucosamine. A rabbit antibody against the protein competed with mannan and mannosylated ferritin for the binding sites. The receptor was localized by immunolabelling on ultrathin frozen sections and the relative density of labelling/cell compartment was calculated. The receptor appeared randomly distributed on the surface. Labelling of coated pits was occasional. A higher density of the gold marker was found on surface infoldings (filopods, lamellopods). Subcellular membranous structures contained few labelled regions, with a relative increase from rough endoplasmatic reticulum to Golgi vacuoles. The highest average density was found on membranes of large vesicles near the surface, presumably derived from lamellopods which fuse at their tips to create an internalized vacuole. Fluorescence micrographs showed the complex folding of plasma processes, sometimes forming crater-like apertures. The particular fluorescence intensity of methanol-fixed cells, due to large vesicles, reflects the amount of receptor which is not exposed on the surface. The extent of receptor-rich membrane involved in formation of surface infoldings, craters and large vesicles indicates their role in receptor traffic in the absence of specific ligands.
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PMID:Immunocytochemical localization of the mannose receptor on ultrathin cryosections of chicken macrophages. 389 46

The initial tissue localization and redistribution of radioactive iron injected intravenously into the rat as ferritin, chondroitin sulfate, and nonviable red cells was determined. Ferritin iron, initially localized in the hepatocyte, showed minimal redistribution over 24 hours in the normal animal. This may be compared with the active release of iron from the reticuloendothelial cell after the intravenous injection of nonviable red cells and chondroitin sulfate iron. All forms of iron were actively mobilized in iron-deficient animals. The effect of chelation of iron by deferoxamine (DFO) on the redistribution pattern over 4 to 6 hours was determined in iron-deficient, normal, iron-loaded, and phenylhydrazine-treated rats to evaluate the effect of iron stores and erythropoiesis. Use of DFO resulted in extensive chelation of radioactive iron within the hepatocyte and greatly reduced the amount of hepatocyte iron available for erythropoiesis. Very little chelation of reticuloendothelial cell-processed iron occurred, and there was little decrease in its utilization for red cell production. Total urinary chelate iron was independent of erythropoiesis but varied in parallel with the iron load of the animal. These studies suggest that DFO does not act on the reticuloendothelial cell but does have at least two sites of action, both of which relate to total storage iron. One involves hepatocyte stores with excretion into the intestinal tract. The other, possibly located at the hepatocyte membrane, results in urinary iron excretion.
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PMID:Storage iron exchange in the rat as affected by deferoxamine. 392 Mar 36


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