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

The incidence of ascorbic acid (AA) deficiency and its effect on serum ferritin concentration relative to body iron stores was studied in 61 unchelated patients with beta-thalassaemia major. Thirty-nine (64%) of patients had subnormal leucocyte ascorbate concentrations without clinical evidence of scurvy. The lowest leucocyte ascorbate concentrations tended to occur in the most transfused patients. No correlation was found between the units transfused and serum ferritin concentration in the AA-deficient patients but a close correlation (r = +0.82; p less than 0.005) existed for the AA-replete group. Similarly a close correlation (r = +0.77; p less than 0.005) was obtained between liver iron concentration and serum ferritin in AA-replete patients but only a weak correlation (r = +0.385; p less than 0.025) existed for the AA-deficient group. When AA-deficient patients were treated with ascorbic acid, serum iron and percentage saturation of iron binding capacity rose significantly; serum ferritin rose in 13 of 21 patients despite the simultaneous commencement of desferrioxamine therapy. In contrast all three measurements tended to fall in AA-replete patients with ascorbic acid and desferrioxamine therapy. Thus, AA deficiency is commonly present in beta-thalassaemia patients with iron overload and may give rise to inappropriate serum ferritin concentrations in relation to body iron stores.
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PMID:Effect of ascorbic acid deficiency on serum ferritin concentration in patients with beta-thalassaemia major and iron overload. 708 92

The absorption of a pharmacological dose of iron was assessed by determination of mucosal uptake, mucosal transfer and retention of 33 mg (Fe(II) as ferrous sulphate and ferrous ascorbate. 20 subjects were studed in a cross-over trial, 11 with normal iron stores and 9 with iron deficiency according to the serum ferritin concentrations. The activity of 59Fe and 51Cr (administered as a non-absorbable indicator) was measured by whole-body counting. There was no difference in absorption between the two iron compounds in normal subjects. Absorption of ferrous ascorbate averaged 52% higher than ferrous sulphate in subjects with iron deficiency. The difference was the result of higher mucosal uptake, probably because oxidation of Fe(II) in the alkaline milieu of the intestine, which leads to formation of non-absorbable Fe(III) complexes, was prevented. The mucosal transfer fraction of both compounds was identical.
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PMID:Mucosal uptake, mucosal transfer and retention of a therapeutic dose of iron. 717 3

The release of iron from horse spleen ferritin by the chelating agents desferrioxamine B, rhodotorulic acid, 2,3-dihydroxybenzoate, 2,2'-bipyridyl and pyridine-2-aldehyde-2-pyridyl hydrazone (Paphy) has been studied in vitro. Ferritin prepared by classical procedures involving thermal denaturation releases its iron less effectively than ferritin isolated by a modified procedure that avoids this step. Desferrioxamine B and rhodotorulic acid are the most effective in releasing iron from both preparations of ferritin. When FMN is added, iron release by desferrioxamine B, rhodotorulic acid, and 2,3-dihydroxybenzoate was effectively blocked, whereas both bipyridyl and Paphy showed a marked simulation. A substantial increase in iron release was also observed for bipyridyl and Paphy with ascorbate; a less important increase was noted for rhodotorulic acid. EDTA exerted a marked inhibition of iron release from ferritin with rhodotorulic acid, 2,3-dihydroxybenzoate, bipyridyl, and Paphy. The effects of citrate and oxalate on iron release by the chelators was small. The effect of the concentration of flavin on iron release from ferritin by bipyridyl and desferrioxamine B have been studied. Desferrioxamine is unable to mobilize FeII from ferritin following reduction by reduced FMN, whereas bipyridyl can rapidly complex the ferrous iron. The results are discussed in the context of our current concepts of storage iron mobilization in the treatment of iron overload.
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PMID:Iron mobilization from ferritin by chelating agents. 719 39

Ferritin from horse spleen was found to cause severe chromosome aberrations in cultured Chinese hamster ovary cells. Ferritin at 15 to 170 microgram/ml was clastogenic and at higher doses was cytotoxic. At comparable concentrations of protein or iron, neither apoferritin nor complexed iron was clastogenic. Sulfhydryl compounds glutathione and cysteine reduced the cytotoxic and clastogenic activities of ferritin. Physiological concentrations of glutathione may normally be sufficient to protect cells from damage. The reducing agent ascorbate had little protective effect. Chelating agents varied in their inhibitory activity: ethylenediaminetetraacetic acid (hexadentate) greater than nitrilotriacetic acid (tetradentate) greater than salicylate (bidentate). 2,2'-Bipyridyl enhance the chromosome-damaging action of ferritin while histidine did not markedly alter the frequencies of aberrations. Catalase and superoxide dismutase showed no inhibitory activity. The mechanism of DNA damage may involve reduction of Fe(III) in the ferritin core to Fe(II), followed by reoxidation of Fe(II) with possible formation of free radicals.
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PMID:Chromosome-damaging activity of ferritin and its relation to chelation and reduction of iron. 719 42

L-(-)-ascorbate mobilizes iron from horse-spleen ferritin in the presence of oxygen at pH 8.0. The reaction is strongly stimulated by Cu2+. Dehydroascorbate and other stable oxidation products of ascorbate are ineffective. We present evidence that monodehydroascorbate mobilizes ferritin iron by reduction.
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PMID:Rapid mobilization of ferritin iron by ascorbate in the presence of oxygen. 740 58

The Department of Health (1992) has recently stated that 'Nutritional reviews concerning elderly people are especially constrained by lack of data', and that much of the emphasis in the nutritional literature has been placed on the study of institutionalized, and often chronically ill, elderly subjects rather than the non-institutionalized elderly who form the majority of this population. The present study presents information on the dietary intake and biochemical status of non-institutionalized elderly subjects (68-73 and 74-90 years) and compares such data with those obtained for adult (20-64 years) and adolescent (13-14 years) populations living within the same community. Nutrient intakes and appropriate biochemical measurements of nutrient status, performed on fasting blood samples, were statistically examined and have been discussed in relation to potential age-related influences. The nutrient intake of elderly subjects was on a par with adolescents of corresponding sex but generally lower than that of adult counterparts. There were several significant differences in biochemical measurements of nutrient status between age groups. In general these did not suggest progressive age-related trends. However, there were significant suggestions of age-related increases in whole-blood glutathione peroxidase (EC 1.11.1.9) activity, serum ferritin, plasma cholesterol, LDL and triacylglycerol concentrations and decreases in plasma HDL and ascorbic acid concentrations. The significance of these differences is discussed. An age-related difference (suggestive of a decline) in vitamin C status together with a difference (suggestive of an increase) in glutathione peroxidase activity may indicate an imbalance in the regulation of O2-derived free-radicals with ageing. These observations are worthy of a further study in the light of current thinking which relates the induction of a number of diseases to oxidative damage.
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PMID:Nutrient intake and biochemical status of non-instutionalized elderly subjects in Norwich: comparison with younger adults and adolescents from the same general community. 757 86

Serum micronutrient levels and their relationship to precancerous gastric lesions were studied in 600 subjects aged 35-64 years living in high-risk area of gastric cancer in Linqu County, Shandong Province. Serum micronutrient levels in local residents were 0.54 micrograms/ml, 0.29 micrograms/ml, 3.14 micrograms/ml, 9.62 micrograms/ml, 30.2 micrograms/L, 924 micrograms/L, 1 016 micrograms/L, and 42.0 micrograms/L for vitamin A, beta-carotene, vitamin C, vitamin E, selenium, zinc, copper and ferritin, respectively. Serum levels of beta-carotene, vitamin C and ferritin, and ratio of serum levels of zinc and copper correlated inversely to severity of pathological changes in gastric mucous membrane. With increase of serum level of beta-carotene or vitamin C, odds ratios (OR) of intestinal dysplasia and metaplasia lowered to 0.8, 0.6 and 0.9, 0.5, respectively, and with increase of those of both beta-carotene and vitamin C, their OR lowered further to 0.16, with patients of chronically atrophic gastritis as controls. It indicated maybe beta-carotene and vitamin C played a strong contributing role in protecting from development of precancerous gastric lesions.
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PMID:[Relationship between serum micronutrients and precancerous gastric lesions]. 758 56

Replenishment of ascorbate in cultured cells, which are almost uniformly vitamin-deficient, increases ferritin mRNA translation in response to iron by 20-fold (Toth, I., Rogers, J. T., McPhee, J. A., Elliott, S. M., Abramson, S. L., and Bridges, K. R. (1995) J. Biol. Chem. 270, 2846-2852). We now demonstrate that ascorbate increases cytosolic aconitase activity. The iron-responsive element-binding protein (IRP-1) exists in three states: bound to mRNA without aconitase activity, free in the cytosol without aconitase activity, and free in the cytosol with aconitase activity. Ascorbate converts free IRP-1 to the enzymatically active form. Enhanced ferritin synthesis with subsequent iron stimulation is due to the altered equilibrium of the free IRP-1. The cellular biology of iron is closely intertwined with that of ascorbate.
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PMID:Ascorbic acid enhances ferritin mRNA translation by an IRP/aconitase switch. 764 38

An intervention study was designed to evaluate the fatty acid (FA) status of children aged 6-11 years before and after iron fortification. Iron-deficient (ID) and matched controls without ID (n = 30) were selected. All children received soup (160 ml) fortified with 20 mg iron and 100 mg vitamin C for 15 weeks on school days. Measurements before and after intervention included dietary intake, haematological and iron status and FA composition of plasma and erythrocyte membranes (EMBs). The prevalence of low plasma ferritin concentration and transferrin saturation decreased in the ID children by 40% and 56%, respectively, with intervention. Plasma FAs reflected dietary FA intake. In comparison with controls, the ID group presented with increased percentage total saturated FAs (SFAs; p = 0.0002) in their EMB phosphatidylcholine (PC) and reduced percentage total polyunsaturated FAs (PUFAs; p = 0.0037) before intervention. Lower total n-3 FAs (p = 0.0070), including eicosapentenoic acid (EPA; p = 0.0034), docosapentenoic acid (DPA; p = 0.0048) and docosahexenoic acid (DHA; p = 0.0058), were observed in the ID group. The EMB phosphatidylethanol-amine (PEA) of the ID children presented with lower percentages of alpha-linolenic acid (ALA; p = 0.0001), EPA (p = 0.0051) and DHA (p = 0.0084) compared to controls before intervention. Iron intervention was associated with an increase (p < 0.05) in the percentage of n-3 FAs in the EMB-PC and EMB-PEA of the ID group to percentages comparable to that in the control group. It appears that iron status can influence FA metabolism of specific n-3 FAs in the EMBs of young children.
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PMID:The effect of iron fortification on the fatty acid composition of plasma and erythrocyte membranes in primary school children with and without iron deficiency. 770 22

An intervention study was designed to evaluate the fatty acid (FA) status of children aged 6-11 years before and after iron fortification. Iron deficient (ID) and matched controls without ID (n = 30) were selected. All children received soup (160 mL) fortified with 20 mg iron and 100 mg vitamin C for 15 weeks on school days. Measurements before and after intervention included dietary intake, haematological and iron status and FA composition of plasma and erythrocyte membranes (EMBs). The prevalence of low plasma ferritin concentration and transferrin saturation decreased in the ID children by 40% and 56%, respectively, with intervention. Plasma FAs reflected dietary FA intake. In comparison with controls, the ID group presented with increased percentage total saturated FAs (SFAs; p = 0.0002) in their EMB phosphatidylcholine (PC) and reduced percentage total polyunsaturated FAs (PUFAs; p = 0.0037) before intervention. Lower total n-3 FAs (p = 0.0070) including eicosapentaenoic acid (EPA; p = 0.0034), docosapentaenoic acid (DPA; p = 0.0048) and docosahexaenoic acid (DHA; p = 0.0058) were observed in the ID group. The EMB phosphatidylethanolamine (PEA) of the ID children presented with lower percentages of alpha-linolenic acid (ALA; p = 0.0001), EPA (p = 0.0051) and DHA (p = 0.0084) compared to controls before intervention. Iron intervention was associated with an increase (p < 0,05) in the percentage of n-3 FAs in the EMB-PC and -PEA of the ID group to percentages comparable to that in the control group. It appears that iron status can influence FA metabolism of specific n-3 FAs in the EMBs of young children.
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PMID:The effect of iron fortification on the fatty acid composition of plasma and erythrocyte membranes in primary school children with and without iron-deficiency. 784 96


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