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

Characteristic cytoplasmic and intranuclear fibrillar bodies were produced, within 24 hours, in epithelial cells of the proximal convoluted renal tubules of rats and mice by injecting a single dose of lead acetate either intraperitoneally (100 mug Pb/g) or into the heart (10 mug Pb/g). The frequency of cytoplasmic fibrillar bodies (CFB) rose during the first 4 days following injection of lead and diminished thereafter. Ten days after intracardiac injection of lead no CFB were found; 10 days after intraperitoneal injection, they were still present, though probably in diminished number. Disappearance of CFB may be related to autophagocytosis. Intranuclear fibrillar bodies did not disappear, perhaps because nuclei lack a lysosomal apparatus. Within the first 3 days after injection of lead, clusters or paracrystalline arrays of ferritin molecules were frequently situated in the immediate vicinity of CRB or abutted against CFB; after the third day, little or no ferritin was found near CFB. Intramuscular injection of iron-dextran complex (50 mg Fe/ml) 24 hours prior to intraperitoneal administration of lead did not increase incidence or size of ferritin clusters in the vicinity of CFB in rats. The presence of ferritin near CFB may have been an indirect consequence of inhibition, by lead, of synthesis of heme prosthetic groups.
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PMID:Evolution of cytoplasmic fibrillar bodies induced by lead in rat and mouse kidneys. 17 27

Conjugates of ferritin with low density lipoproteins (LDL) were prepared and separated by sucrose gradient centrifugation. These conjugates, at cholesterol concentration of 100--132 microgram/ml, caused a greater than 90% suppression of hydroxymethylglutaryl coenzyme A reductase activity and of acetate incorporation into cholesterol in cultured skin fibroblasts from a normal subject as well as from a subject with homozygous familial hypercholesterolemia. The half maximal inhibition concentration was approx. 10 microgram/ml cholesterol for LDL and ferritin . (LDL)2 and 5 microgram/ml for (ferritin)2 . LDL in both cell lines. In contrast, native low density lipoproteins have only a minimal inhibitory effect in homozygous cells. The ability of the conjugates to stimulate the incorporation of oleate into cholesteryl esters was also equal in the two cell lines, although the conjugates were only 10% as active as low density lipoproteins in the normal cells. LDL reduced the ferritin . (LDL)2-mediated suppression of hydroxymethylglutaryl-CoA reductase activity in homozygous cells while ferritin . (LDL)2 reduced the LDL-mediated stimulation of cholesteryl ester formation in normal cells.
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PMID:Suppression of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity and of incorporation of acetate into cholesterol in homozygous hypercholesterolemic fibroblasts by ferritin-low density lipoprotein conjugates. 20 53

Horseradish peroxidase (HRP) uptake was used to measure fluid-phase pinocytosis in monolayers of human epithelioid carcinoma cells (A-431). Histochemistry confirmed that cell-associated HRP was restricted to intracellular vesicles. Biochemical methods showed that HRP uptake in control cultures was directly proportional to the duration of exposure. The addition of low concentrations of epidermal growth factor (EGF) to the incubation media produced a 10-fold increase in the initial rate of pinocytosis. The EGF effect was rapid (within 30 s) but transient; the rate of pinocytosis returned to control levels within 15 min. Metabolic inhibitors reduced the EGF-stimulated rate of pinocytosis by greater than 90%. A conjugate of EGF and ferritin (F:EGF) was used to simultaneously compare the intracellular locations of EGF and HRP. Much of F:EGF was internalized in approximately 100-nm vesicles, while most of the HRP was located in much larger vesicles (range 0.1--1.2 micrometer) which also contained F:EGF. The tumor-promoter 12-0-tetradecanoyl-phorbol-13-acetate, which shares several biological activities with EGF, was also effective in stimulating an increase in the rate of pinocytosis.
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PMID:Rapid stimulation of pinocytosis in human carcinoma cells A-431 by epidermal growth factor. 31 44

The existent labelling materials for studies of antigen--antibody interaction at ultrastructural level, namely ferritin and peroxidase, because of their large molecular size do not fulfill all requirements of excellent markers for electron microscopy (EM). Uranyl acetate has a molecule 354 times smaller than IgG and its uranium atom is electron-dense. These physical characteristics of uranyl acetate make it a labelling material par excellence as described in this article. Quantitative and qualitative studies of Rh antigen-antibody interactions are for the first time presented at the ultrastructural level, and the application of the uranyl-labelled antibody (ULA) method for weak antisera (dilutions 100 to 1000 time higher than the Coombs range of sensitivity) is demonstrated. The ULA method opens a new era for studies of antigens, antibodies and their interactions because it will demonstrate visibly details of the antigen-antibody interaction and is especially suitable for studies of weak antisera.
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PMID:Uranyl-labelled antibody (ULA) method and its application for Rh antibodies. 41 69

Low density lipoprotein (LDL) oxidation mediated by phorbol myristate acetate (PMA)- and formylmethionylleucylphenylalanine (FMLP) -stimulated human neutrophils was enhanced by 70% in the presence of ferritin. Iron released from ferritin by the superoxide anion generated in the respiratory burst of stimulated neutrophils is shown to be involved in lipoprotein oxidation. Ascorbate (100 microM), superoxide dismutase (10 micrograms/ml) and uric acid (430 microM) showed inhibitory effects of 30% [corrected], 70% and 50% on LDL oxidation, respectively. Ceruloplasmin (2.7 microM) potentiated LDL oxidation by stimulated neutrophils and ferritin, both alone and in the presence of methionine. Methionine (1 mM) and catalase (30 micrograms/ml) increased LDL oxidation by stimulated neutrophils and ferritin. These data suggest that LDL oxidation by stimulated neutrophils and ferritin may be relevant in inflammation when both neutrophils and ferritin are increased.
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PMID:Low density lipoprotein oxidation by stimulated neutrophils and ferritin. 133 54

The role of iron in allyl alcohol-induced lipid peroxidation and hepatic necrosis was investigated in male NMRI mice in vivo. Ferrous sulfate (0.36 mmol/kg) or a low dose of ally alcohol (0.6 mmol/kg) itself caused only minor lipid peroxidation and injury to the liver within 1 h. When FeSO4 was administered before allyl alcohol, lipid peroxidation and liver injury were potentiated 50-100-fold. Pretreatment with DL-tocopherol acetate 5 h before allyl alcohol protected dose-dependently against allyl alcohol-induced lipid peroxidation and liver injury in vivo. Products of allyl alcohol metabolism, i.e. NADH and acrolein, both mobilized trace amounts of iron from ferritin in vitro. Catalytic concentrations of FMN greatly facilitated the NADH-induced reductive release of ferritin-bound iron. NADH effectively reduced ferric iron in solution. Consequently, a mixture of NADH and Fe3+ or NADH and ferritin induced lipid peroxidation in mouse liver microsomes in vitro. Our results suggest that the reductive stress (excessive NADH formation) during allyl alcohol metabolism can release ferrous iron from ferritin and can reduce chelated ferric iron. These findings provide a rationale for the strict iron-dependency of allyl alcohol-induced lipid peroxidation and hepatotoxicity in mice in vivo and document iron mobilization and reduction as one of several essential steps in the pathogenesis.
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PMID:NADH-dependent reductive stress and ferritin-bound iron in allyl alcohol-induced lipid peroxidation in vivo: the protective effect of vitamin E. 173 Jan 48

We have recently characterized an adipocyte cDNA (clone 5) that is enhanced in expression by environmental and hormonal conditions favoring adipogenic differentiation. Moreover, certain agents including fibroblast growth factor and phorbol 12-myristate 13-acetate (but not epidermal growth factor) markedly inhibit clone 5 gene expression and prevent TA1 cell differentiation. These results led us to propose that a threshold level of the clone 5 gene product (AP27 protein) is required for triggering adipocyte differentiation. We have constructed vectors that direct the synthesis of clone 5 antisense RNA to reduce the levels of AP27 in adipogenic cell lines TA1 and 3T3-L1. We show here that when these cells express clone 5 antisense RNA, they fail to undergo morphological differentiation, whereas adipogenesis is unaffected in cells expressing antisense beta-actin or ferritin heavy-chain RNA. We further show that cells expressing clone 5 antisense RNA (but not the other antisense RNAs) are unable to induce the expression of characteristic "adipocyte-specific" mRNAs. The level of inhibition of differentiation by clone 5 antisense RNA correlates with decreased levels of AP27 protein. These results provide strong evidence that expression of AP27 is linked to adipogenic differentiation and that AP27 may be a component of an as-yet-uncharacterized signal-transduction pathway required for the triggering of adipocyte differentiation.
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PMID:Reduced expression of AP27 protein, the product of a growth factor-repressible gene, is associated with diminished adipocyte differentiation. 173 87

The aim of this study was to determine the crude prevalence of alpha-thalassemia traits in Taiwan. A total of 1435 healthy employees from a statewide company were randomly screened by complete blood count determination with indices. Subjects with mean corpuscular volume less than 80 fl were analyzed by hemoglobin electrophoresis on cellulose acetate to exclude beta-thalassemia and with serum ferritin to exclude iron deficiency. Modified hemoglobin H inclusion staining was performed to confirm the diagnosis of alpha-thalassemia traits, and DNA probe studies were used to confirm the validity of this test. The overall prevalence rate of alpha-thalassemia trait was 3.4% (48 out of 1435). In persons of mainland Chinese origin, prevalence was 0.4%, and among persons of Taiwanese origin, it was 4.0% (47 out of 1171). We conclude that alpha-thalassemia traits are common genetic disorders in Taiwan and that antenatal screening is advised to reduce the frequency of occurrence of hemoglobin Bart's hydrops fetalis. The methods we used proved to be reliable and inexpensive.
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PMID:Alpha-thalassemic traits are common in the Taiwanese population: usefulness of a modified hemoglobin H preparation for prevalence studies. 174 8

The development of ultrahigh-resolution scanning electron microscopes (SEMs) has made the observation of biological macromolecules feasible, but adequate preparation methods have not yet been established. Although it has been possible to observe some molecules after they have been spread on a carbon substrate, this method has not proved suitable for other molecules which exhibit lower contrast, or are more susceptible to damage by the electron beam. In this study we have applied heavy-metal impregnation methods using phosphotungstic acid, uranyl acetate, or osmium tetroxide mordanted by tannic acid. In addition, contamination due to the electron beam was reduced by improving the vacuum in the specimen chamber, and by the use of a heated specimen stage. Using these measures, haemocyanin, ferritin, apoferritin, thyroglobulin and immunoglobulin M were successfully image. Ultrahigh-resolution SEM seems likely to become an important means for studying the morphology of biological macromolecules.
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PMID:Application of high-resolution scanning electron microscopy to biological macromolecules. 192 Mar 94

Lipid peroxidation of erythrocyte membrane was caused by phorbol myristate acetate (PMA)-stimulated polymorphonuclear leukocytes (PMN) in the presence of ferritin. PMN themselves were not peroxidized. A lag period was observed before the start of the peroxidation reaction. In contrast, ferritin iron was continuously released by PMA-stimulated PMN, suggesting that accumulation of free iron in the reaction system was important for proceeding of the peroxidation reaction. Superoxide dismutase, catalase, hydroxyl radical scavengers and an iron chelator, diethylenetriaminepenta-acetic acid, inhibited the lipid peroxidation, indicating that the lipid peroxidation is initiated by a hydroxyl radical generated from the interaction of H2O2 with ferrous iron released from ferritin.
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PMID:Lipid peroxidation of the erythrocyte membrane caused by stimulated polymorphonuclear leukocytes in the presence of ferritin. 193 70


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