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

The localization of complex carbohydrates in the Golgi apparatus, secretory granules and plasmalemma of mouse parotid acinar cells was studied using the fracture-labelling method. The hexose residues of glycoconjugates were identified using ferritin conjugated with Wheat Germ Agglutinin (WGA-), Ricinnus Communis Agglutinin II (RCA-II-), Phaseolus Vulgaris Agglutinin (PHA-) and Limulus Polyphemus Agglutinin (LPA-). We found that the fracture-labelling method allows not only the labelling of membrane faces but also analysis of the compartment's content that is exposed during the fracturing of the tissue. Our results revealed differences in the hexose residues located in the Golgi apparatus, secretory granules and the apical and lateral plasmalemma. Numerous binding sites for WGA-, PHA- and RCA-II-ferritin were demonstrable in the Golgi apparatus. In secretory granules, the WGA- and RCA-II-ferritin binding sites were most numerous, while LPA-ferritin binding sites were very rare. The density of the binding sites for PHA-ferritin showed considerable variation in secretory granules. The apical plasmalemma exhibited a high density of binding sites for all of the lectins used. In the lateral plasmalemma, LPA-ferritin was not bound, and there were fewer binding sites for WGA-, RCA-II- and PHA-ferritin.
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PMID:Lectin-binding pattern in parotid acinar cells. The fracture-labelling method and post-embedding staining. 243 Sep 21

Serum ferritin and diabetes control were evaluated in 18 White patients with poorly controlled type II (non-insulin-dependent) diabetes who had no known causes of iron-storage disorder. Serum ferritin levels were found to be elevated with normal serum iron and total iron-binding capacity in 9 of the 18 patients studied. Because excess iron, typified by hemochromatosis, is associated with diabetes, and diabetes has been shown to improve after lowering total-body iron load through repeat venesection, I investigated whether regulating elevated ferritin levels could facilitate diabetes control. Deferoxamine (DFO), a known specific chelator of iron, was used because of its capacity to correct excess iron stores. All 9 patients in the high-ferritin diabetic group and 7 of 9 diabetic control subjects with normal serum ferritin levels were given DFO (10 mg/kg i.v.) twice weekly. Diabetic control, fasting glucose, triglyceride, cholesterol, HbA1c, and serum ferritin levels were monitored. Data show that lowering elevated ferritin levels correlated well with diabetes control and improved fasting glucose, triglyceride, and HbA1c in 8 of 9 patients with high ferritin levels. Lowering normal ferritin levels had no effect on diabetes control or on any of the other parameters in the 7 control subjects. This study shows there is a need to study iron metabolism in poorly controlled diabetes and demonstrates the value of DFO in controlling high-ferritin diabetes.
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PMID:Deferoxamine therapy in high-ferritin diabetes. 279 74

Ferric nitrilotriacetate, which causes in vivo organ injury, induced lipid peroxidation and cell death in Ehrlich ascites tumor cells in vitro. The process was inhibited by butylated hydroxyanisole and enhanced by vitamin C and linolenic acid, indicating a close relationship between cytotoxicity and the lipid peroxidizing ability of Fe3+ NTA. The cytotoxicity was suppressed by glucose and a temperature below 20 degrees C. Lipid peroxidation of Fe3+ NTA-treated cells was greater at 0 degree C than at 37 degrees C, contrary to results with Fe3+ NTA-treated plasma membranes of Ehrlich ascites tumor cell. These results suggested that metabolism and membrane fluidity are important factors in the expression of the Fe3+ NTA-induced cytotoxicity. H2O2 showed a lower cytotoxicity than did Fe3+ NTA but a greater lipid peroxidizing ability. H2O2 appeared to damage the cells less, and was quenched rapidly by cellular metabolism unlike Fe3+ NTA. In transferrin-free medium, Ehrlich ascites tumor cell readily incorporated Fe3+ NTA, and iron uptake was greater than NTA-uptake in Fe3+ NTA-treated cells, suggesting that Ehrlich ascites tumor cell incorporated iron from Fe3+NTA and metabolized it into an inert form such as ferritin.
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PMID:Lipid peroxidation and cytotoxicity of Ehrlich ascites tumor cells by ferric nitrilotriacetate. 287 31

We determined the catalytic concentration of gamma-glutamyltransferase in serum from a population sample of 1408 women in seven age strata between 26 and 72 years. The range in healthy individuals for the different age groups was found to increase with age with a maximum of the central 0.95 fractile interval at 58 years (0.17-1.68 microk/l). The serum gamma-glutamyltransferase activity correlated with body mass index, blood pressure and concentrations of blood glucose and serum ferritin, triglycerides and cholesterol. During follow-up of women with gamma-glutamyltransferase activity greater than 1.20 microk/l, no woman developed any disease possibly related to the original finding of raised serum gamma-glutamyltransferase activity, several individuals being apparently healthy. Apparently, the serum gamma-glutamyltransferase assay is an unspecific indicator of several metabolic abnormalities. High values may be found in individuals in whom all commonly done investigations have given results within the health-associated reference interval.
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PMID:Serum gamma-glutamyltransferase in a Swedish female population. Age-related reference intervals; morbidity and prognosis in cases with raised catalytic concentration. 290 Nov 86

Oral glucose tolerance tests were conducted in 29 patients with aplastic anemia and 20 nondiabetic controls. Seventeen were men and 12 were women, ranging in age from 15 to 67 years. Based on the results of oral glucose tolerance test, the patients were divided into three groups: 14 previously treated cases with normal glucose tolerance; eight previously treated cases with abnormal glucose tolerance, of whom six had diabetes and two had impaired glucose tolerance; and seven newly diagnosed cases with normal glucose tolerance. Hyperinsulinemia and insulin resistance were observed in all patients. Multivariate analyses show that sex, age, body mass index, previous androgen and corticosteroid therapy, previous blood transfusion, initial hemoglobin and white blood cell and serum ferritin concentrations were not significantly related to hyperinsulinemia as expressed by the integrated insulin area under the curve of glucose tolerance test. Patients in the second group who had abnormal glucose tolerance had a delay in insulin secretion in response to glucose, indicating a deterioration of insulin reserve in the beta cells. Patients in this group were significantly older at the time of diagnosis than those in the first group. No other determinants of the development of abnormal glucose tolerance were demonstrated.
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PMID:Glucose intolerance, hyperinsulinemia and insulin resistance in aplastic anemia. 291 40

Dietary supplementation with high-carbohydrate, guar gum fiber (HCF) is effective in acutely blunting postprandial blood glucose levels. We report the effect of such supplementation on the diet and nutritional status of a group of 16 subjects with non-insulin-dependent diabetes mellitus (NIDDM) who incorporated either HCF bars (35.7 g carbohydrate and 6.6 g guar gum/bar) or placebo bars (identical except for the absence of guar gum) into the diet for 6 mo as part of a double-blind, randomized clinical trial. The HCF subjects achieved mean daily intake of 4.8 +/- 0.4 bars, constituting 51.2 +/- 3.1% of total calories and providing 29.7 +/- 2.6 g guar gum daily. Energy intakes and body weight did not change significantly in either group. Food consumption patterns and nutrient intakes did change, although not enough to impair the nutritional integrity of the diet because the bars themselves served as a source of nutrients. The bars were rich in thiamin, B6, folacin, phosphorus, iron, zinc, and copper, adequately replacing any decrease in nutrient intake as a result of foods being dropped from the diet. In fact, daily intakes of B6, folacin, and copper actually increased due to contributions from the bars. Nutrients in which the bars were poor (vitamins A, C and B12) resulted in suboptimal intakes (less than 66% RDA). Although no significant change in nutritional status of the HCF group occurred as determined by arm muscle area, arm fat area, hemoglobin, hematocrit, or serum albumin, transferrin, iron, ferritin, calcium, phosphate, B12, and magnesium levels, these indicators of nutritional status are rather insensitive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nutritional risk of high-carbohydrate, guar gum dietary supplementation in non-insulin-dependent diabetes mellitus. 302 7

The biological activity and morphological distribution of protein A on the cell surface were studied in a medium containing an excess of either mannitol or glucose, which suppressed protein A production of Staphylococcus aureus, Cowan I strain. Preculture of the organisms in the presence of a sugar suppressed the expression of protein A, resulting in a decrease in the number of cells bound with antiferritin rabbit IgG molecules, which specifically indicate protein A distribution. The distribution pattern of protein A on the cell surface changed with glucose but not with mannitol. The two-layered ferritin distribution on the organism grown in the control medium was altered into a heavily labeled, thick and rough layer with glucose, suggesting the induction of a conformational change in the polypeptide chain forming protein A. This was positively supported by the increase in trypsin susceptibility of protein A.
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PMID:Effect of mannitol and glucose on the distribution and trypsin susceptibility of protein A of Staphylococcus aureus. 309 33

To test the hypothesis that deficiencies in hypothalamic-pituitary function in genetic hemochromatosis result from cellular injury by iron deposits, we conducted provocative tests in 11 men with genetic hemochromatosis before and after iron depletion by serial phlebotomy and in 10 control subjects. We gave combination intravenous injections of insulin (0.15 U/kg), luteinizing hormone releasing hormone (LHRH, 100 micrograms), and thyrotropin releasing hormone (400 micrograms) and then measured plasma glucose, growth hormone, corticosteroids, follicle-stimulating hormone, luteinizing hormone, prolactin, and thyroid-stimulating hormone at 30-minute intervals for 90 minutes. Phlebotomy caused a substantial decrease in median values for serum ferritin, deferoxamine-chelatable iron, and hepatic iron concentration. Before phlebotomy, stimulation by hypoglycemia and thyrotropin releasing hormone caused significantly less secretion of growth hormone (P = 0.004) and prolactin (P = 0.03) in patients than in control subjects. No significant improvement was noted, however, in growth hormone or prolactin secretion after phlebotomy. Of the 11 patients, 7 had secondary hypogonadism, and phlebotomy did not improve the serum testosterone, follicle-stimulating hormone, luteinizing hormone, or responses to LHRH in any case. Chlorpromazine injections failed to elevate serum prolactin in all patients, and administration of levodopa caused a partial reduction in serum prolactin; thus, the hypothalamus may be an important locus of endocrine malfunction in these patients. We conclude that abnormal hypothalamic-pituitary function in genetic hemochromatosis is not substantially improved by iron-depletion therapy.
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PMID:Influence of phlebotomy treatment on abnormal hypothalamic-pituitary function in genetic hemochromatosis. 310 26

Rabbit muscle phosphoglucomutase was irreversibly inactivated upon preincubation with vitamin C (Vit C). Fe(III), NADH.NADH oxidase.Fe(III), or ferritin.Vit C. Substrate, glucose 1-phosphate and Mg2+ afforded partial protection. No altered amino acid could be detected in the inactive enzyme. Enzyme so inactivated was more susceptible to trypsin. More importantly, during inactivation, the enzyme lost up to 70% of its enzyme-bound phosphate; the completely inactivated enzyme retained the remainder of the bound phosphate which was isolatable as phosphoserine residing in the 22-amino acid long tryptic peptide. Free phosphoserine as well as those in phosphorylase alpha and phosphocasein were resistant to the oxidizing system, suggesting that the phosphoserine of phosphoglucomutase is uniquely vulnerable to these treatments. Alternatively, a fraction of the total 1 mol of phosphate in the phosphoform of phosphoglucomutase may not be associated with phosphoserine. Phosphoglyceromutase, which has phosphohistidine at its active site, was also inactivated by the oxidizing system. However, it did not release any of the bound phosphate.
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PMID:Vit C.Fe(III) induced loss of the covalently bound phosphate and enzyme activity of phosphoglucomutase. 315 31

The differentiation of bacterial from aseptic meningitis in postoperative neurosurgical patients has traditionally been based on the clinical setting, a recent history of steroid administration, and cerebrospinal fluid (CSF) studies, including the total and differential leukocyte counts, Gram stain, glucose, and total protein. Recent reports questioning both the validity of a relative CSF lymphocytosis in excluding bacterial meningitis and the usefulness of standard CSF testing prompted the authors to reevaluate these standard criteria. The type of operation, the presence of a foreign body, use of steroids, postoperative day on which symptoms developed, altered mental status, neck stiffness, headache, and nausea were not helpful in the differential diagnosis. High fever, new neurological deficits, an active CSF leak, and elevated leukocyte counts in the CSF and peripheral blood favored a bacterial etiology. The CSF glucose level and the differential leukocyte count were less helpful. No criterion or combination of criteria was sensitive and specific enough to reliably differentiate aseptic from bacterial meningitis in the majority of patients. The possibility of improving diagnostic accuracy with newer tests, such as CSF lactate, ferritin, total amino acids, C-reactive protein, and amyloid-A, should be assessed.
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PMID:Differentiation of aseptic and bacterial meningitis in postoperative neurosurgical patients. 318 29


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