Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The known relationship between ethanol and the two main proteins of iron metabolism, transferrin and ferritin, are reviewed. Transferrin synthesis decreases in alcoholic cirrhosis, and increases in alcoholic fatty liver. In the latter case, its turnover is accelerated. Serum desialylated transferrin increases in chronic alcoholism and could be the best marker of heavy drinking. The increased uptake of desialylated transferrin by the liver could explain the development of hepatic siderosis in some alcoholics. Serum ferritin increases in chronic alcoholism, much more because of liver damage than in relation to iron stores. It is clear in this review that few experimental studies have been interested in the investigation of these relationships.
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PMID:[Interactions of alcohol and iron proteins]. 265 33

We tested the hypothesis that the hepatic siderosis that characterizes sporadic porphyria cutanea tarda is due to the presence of HLA-linked hemochromatosis alleles. We studied 21 probands with sporadic porphyria cutanea tarda and 135 of their relatives by determining HLA haplotypes and measuring transferrin saturation and serum ferritin concentration. Liver biopsies were performed in all probands and in relatives when appropriate. Seventeen pedigrees were available and were studied by both likelihood analysis and by a gene counting method. We estimated that 10 of the 17 probands with available living relatives possessed at least one hemochromatosis allele. Thirteen of the 21 probands (62%) possessed at least one HLA-A3 alloantigen. Eighteen of 69 relatives who shared an HLA haplotype with a proband (26%) had an elevation of transferrin saturation or serum ferritin concentration. Only one first-degree relative not sharing an HLA haplotype with a proband had an elevated transferrin saturation or serum ferritin concentration. These findings indicate that HLA-linked hemochromatosis alleles are far more common in patients with sporadic porphyria cutanea tarda than in individuals in the general population and may be responsible for the hepatic siderosis associated with most cases of sporadic porphyria cutanea tarda.
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PMID:HLA-linked hemochromatosis alleles in sporadic porphyria cutanea tarda. 278 60

Impaired utilization of iron by the heme synthesizing red cell precursors was investigated in 258 patients with malignant tumors of different histological types and different tumor spread. There was evidence, that impaired iron uptake by the erythropoietic cells results in an increased flow of iron to the reticuloendothelial iron stores. Investigations on bone marrow smears showed that sideroblast counts were significant lower than in healthy controls reflecting a deficient iron supply to the erythropoietic cells. In contrast, reticuloendothelial storage iron was increased paralleled by an increased serum ferritin concentration. Both abnormalities correlated with the malignancy and the stage of the tumor. It could be demonstrated that the degree of the hyperferritinemia paralleled very closely the severity of the anemia becoming more pronounced with increasing tumor mass. This parallelism indicates that the siderosis is pathophysiologically related to the defect of erythropoiesis observed in malignant disease. Since the iron uptake by the erythropoietic cells is mediated by transferrin in a further series of experiments the serum transferrin concentration was investigated in malignant diseases. There was found a close inverse correlation between serum transferrin concentration and serum ferritin concentration. This correlation supports the concept of a defect in erythropoiesis due to an impaired transferrin mediated iron supply caused by tumor induced hypotransferrinemia. This defect is responsible for a shift of iron to the iron stores and a secondary siderosis.
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PMID:[Anemia in malignant tumor diseases. VI. Secondary siderosis caused by the shift of iron, unused for hemoglobin synthesis, into iron stores]. 281 66

The authors have investigated the hypothesis that neonatal hemochromatosis (NH), a generally fatal disease of infancy, is due to abnormalities in cellular response to ambient levels of iron. The clinical and necropsy findings in two infants with NH, the results of evaluations for iron-storage disease in their first-degree relatives, and the results of the authors' studies of ferritin and transferrin-receptor (TfR) synthesis in NH and normal fibroblasts are presented. No differences between cultured skin fibroblasts from a normal infant and similar cells from the two infants with NH were seen with respect to TfR and ferritin synthesis rates or their modulation by iron. NH and adult idiopathic hemochromatosis (AH) share a pattern of siderosis in which epithelial and mesenchymal elements contain large quantities of stainable iron, while reticuloendothelial elements contain almost none. Although no familial correlation between NH and AH has been established, and none appeared to exist in these two families, the authors' results parallel those of previous studies of various cell types from persons with AH. The abnormalities in cellular iron handling, undefined at present, that are associated with the phenotype common to NH and AH do not appear primarily to involve the regulation by iron of rates of TfR and ferritin synthesis.
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PMID:Neonatal hemochromatosis. The regulation of transferrin-receptor and ferritin synthesis by iron in cultured fibroblastic-line cells. 291 54

The distribution of iron and mycobacteria was examined in the intestinal tract of ruminants with naturally-occurring M. paratuberculosis infection and compared with mycobacterial infections in several species. This distribution was compared with that of iron in chronic lesions caused by other microbial or parasitic agents. In the clinical form of paratuberculosis in cattle, sheep and goats there was marked lymphangiectasis and a high proportion of the granulomatous lesions contained siderotic macrophages with a high mycobacterial content. In cattle with preclinical lesions of granulomatous enteropathy, the greatest number of acid-fast organisms was present in siderotic, non-differentiated, ileo-caecal macrophages; concurrent mast cell-associated allergic enteropathy was also apparent in the duodenum, proximal and mid-ileum of most animals. In paratuberculosis-affected herds, a high proportion of non-productive cows were without classical granulomatous change but had cultural or immunological evidence of M. paratuberculosis infection and similar allergic catarrhal enteropathy of the upper intestinal tract. Interstitial haemorrhage of the ileocaecal valve, with the accumulation of haemosiderin and ferritin in undifferentiated macrophages was observed in some of these cattle and also in others with experimentally-induced copper deficiency and acute ostertagiasis. Colonisation of the ileo-caecal or caecal glandular crypts by large, apparently saprophytic acid-fast organisms indicated regional tolerance to such organisms in all cattle. In other mycobacterioses such as bovine or avian tuberculosis, undifferentiated, siderotic macrophages containing mycobacteria were also seen in early granulomas, but epithelioid and giant cell differentiation invariably led to the disappearance of intracellular iron and a reduction in mycobacterial numbers. In possums in which epithelioid and giant cells did not occur in response to M. bovis infection, siderosis persisted in many macrophages and overwhelming mycobacterial multiplication occurred. These studies indicate that, in most infections with mycobacteria, differentiation of macrophages radically reverses their iron acquisitive properties, creating an intracellular environment unsuitable for mycobacterial multiplication. It seems likely that allergically mediated microvascular haemorrhage, local tolerance of commensal mycobacteria and attenuation of the macrophage siderosis reversal mechanism provide unique conditions for early, uninhibited, intracellular multiplication of M. paratuberculosis in the ileo-caecal valve of certain mature ruminants.
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PMID:Intracellular iron storage and the pathogenesis of paratuberculosis. Comparative studies with other mycobacterial, parasitic or infectious conditions of veterinary importance. 334 90

Brain tissue from five patients with superficial siderosis of the central nervous system was examined by immunocytochemistry for ferritin, glial fibrillary acidic protein (GFAP), alpha 1-antitrypsin, and alpha 1-antichymotrypsin, and by lectin affinity cytochemistry with biotinylated Ricinus communis agglutinin-1 (RCA-1). The sections were pretreated with 2,2'-dipyridyl and sodium hydrosulfite to remove iron and to reveal the antigenic sites. In siderotic cerebellar cortex, ferritin reaction product occurred in the hemosiderin matrix, the cell bodies and processes of Bergmann glia, and in microglia. Astrocytes other than Bergmann glia did not contain ferritin reaction product. RCA-1 stained microglia and hemosiderin whereas antisera to alpha 1-antitrypsin and alpha 1-antichymotrypsin only reacted with iron-depleted granules. The selective vulnerability of the eighth cranial nerve was explained by the presence of ferritin-reactive and lectin-positive microglia. Hemosiderin isolated from frozen cerebellum contained ferritin, GFAP, and vimentin. The presence of the intermediate filament proteins was likely due to co-localization with hemosiderin granules in Bergmann glia. The ability of the brain to biosynthesize ferritin in response to prolonged contact with hemoglobin iron is thought to be the most important factor in the pathogenesis of superficial siderosis. The great severity of the lesion in the exposed cerebellar cortex is readily explained by accelerated ferritin biosynthesis in Bergmann glia.
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PMID:Brain hemosiderin and superficial siderosis of the central nervous system. 336 57

A 32 year old woman with severe aplastic anaemia required frequent transfusions and consequently developed hyperferrioxaemia (54 microMol/l) and hyperferritinaemia (1,700 ng/ml). For the treatment of transfusion siderosis she was given 18 high dose courses each comprising 35 g of desferrioxamine. Because of pre-existing thrombocytopenia (platelet count 5 X 10(9)/l) the iron chelating agent was given by continuous intravenous infusion over 3 1/2 days. High dose desferrioxamine had to be abandoned because of severe bone pain. The desferrioxamine infusions achieved a negative iron balance, iron loss after each infusion being 100 to 200 mg in the urine and 400 mg in the faeces. Serum iron and ferritin concentrations fell almost to normal. This report shows that faecal iron excretion must be taken into account in assessing the balance of iron input and output during desferrioxamine treatment.
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PMID:High dosage desferrioxamine therapy in a female patient with acquired aplastic anaemia and transfusion siderosis. 363 32

A minor electrophoretically fast component was found in ferritin from iron-loaded rat liver in addition to a major electrophoretically slow ferritin similar to that observed in control rats. The electrophoretically fast ferritin showed immunological identity with the slow component, but on electrophoresis in SDS it gave a peptide of 17.3 kDa, in contrast with the electrophoretically slow ferritin, which gave a major band corresponding to the L-subunit (20.7 kDa). Thus the electrophoretically fast ferritin resembles that reported by Massover [(1985) Biochim. Biophys. Acta 829, 377-386] in livers of mice with short-term parenteral iron overload. The electrophoretically fast ferritin had a lower iron content (2000 Fe atoms/molecule) than the electrophoretically slow ferritin (3000 Fe atoms/molecule). Removal and re-incorporation of iron was possible without effect on the electrophoretic mobility of either ferritin species. On subcellular fractionation the electrophoretically fast ferritin was enriched in pellet fractions and was the sole soluble ferritin isolated from iron-laden secondary lysosomes (siderosomes). The amount and relative proportion of the electrophoretically fast species increased with iron loading. Haemosiderin isolated from siderosomes was found to contain a peptide reactive to anti-ferritin serum and corresponding to the 17.3 kDa peptide of the electrophoretically fast ferritin species. Unlike the electrophoretically slow ferritin, the electrophoretically fast ferritin did not become significantly radioactive in a 1 h biosynthetic labelling experiment. We conclude that the minor ferritin is not, as has been suggested for mouse liver ferritin, 'a completely new species of smaller holoferritin that represents a shift in the ferritin phenotype' in response to siderosis, but a precursor of haemosiderin, in agreement with the proposal by Richter [(1984) Lab. Invest. 50, 26-35] concerning siderosomal ferritin.
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PMID:Siderosomal ferritin. The missing link between ferritin and haemosiderin? 366 70

A low molecular weight iron-binding substance that promotes bacterial growth in vitro by increasing iron availability was identified in human blood and urine. Partial purification and physical characterization indicate that this factor is similar to the host-associated iron transfer factor (HAITF) previously isolated from mammalian tissue. HAITF was found to be significantly elevated in the blood of patients with thalassemia who have transfusional siderosis. The level of HAITF in the blood of these patients was also found to correlate with that of serum iron and serum glutamic-oxaloacetic transaminase (SGOT) but not with that of serum ferritin. Thus, elevated blood levels of HAITF may explain the increased susceptibility to infection seen in patients with iron overload. Its physiologic role, however, may involve the transport of iron within cells.
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PMID:Host-associated iron transfer factor in normal humans and patients with transfusion siderosis. 370 Nov 90

Liver function has been evaluated in 74 patients (aged 9 months to 19 years) with beta-thalassemia major. They were selected from 212 patients because their transaminase levels were three times higher than normal for over three months. In 36 of these subjects BSF clearance test was performed. In the majority of patients (70%) average GPT serum values were increased (66.33 +/- 35.41 U/L) while only a few of the youngest age group exhibited normal values. The transaminase level showed a direct relationship with age, ferritin level and transfusional iron. Furthermore a direct correlation was found between iron and gamma globulin levels both being related to age. Test for viral hepatitis markers showed that 60% of all the subjects studied had had HBV infection. Twenty-six of the 36 patients who underwent BSF test had normal values in the first part of the clearance curve, 8 others showed moderate changes while only the 2 remaining revealed severe alterations. The second part of the curve was abnormal in 34 and markedly altered in 2 subjects. Mean GPT serum values correlated with the first part of BSF clearance curve and BSF 45' values correlated with transfused iron. Siderosis, fibrosis, chronic inflammatory infiltration and vacuolar degeneration were seen at liver biopsy. Histological findings of chronic aggressive hepatitis were shown in two patients with high transaminase and gammaglobulin levels who had markedly abnormal BSF curve.
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PMID:[Hepatic pathology in beta-thalassemia major]. 372 17


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