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

We report an apparently protective effect of vitamin A in infants who received iron supplements (15 mg/d) for 3 mo. Those receiving iron showed increases in hemoglobin (8 g/L), ferritin (3.7 micrograms/L), and the acute-phase protein alpha 1-antichymotrypsin (ACT; 0.06 g/L). In both the placebo and iron-supplemented groups there were increases in plasma retinol, lutein, alpha-tocopherol, immunoglobulin A, and immunoglobulin G. The improvement in vitamin A status could only have been from a seasonal increase in dietary sources of vitamin A, eg, breast milk and early weaning foods, and there were no obvious effects on iron utilization (hemoglobin concentrations). However, in the infants receiving iron, those whose retinol concentrations increased also showed reductions in ACT, ferritin, immunoglobulin A, and immunoglobulin M. Vitamin A is well known for its antiinfective properties and we suggest that these observations illustrate the importance of even small increases in dietary vitamin A or differences in vitamin A status in reducing the potentially toxic effects of iron supplements in persons in developing countries. These conclusions should now be confirmed with an intervention study to show that the benefits of vitamin A on iron status are due to reduced levels of infection.
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PMID:Effect of improved vitamin A status on response to iron supplementation in Pakistani infants. 890 3

Plasma retinol and indices of iron status were measured in 148 school children (6-12 years) receiving a soup fortified with iron and vitamin C for a period of 15 weeks. The most significant change in serum iron (P = 0.0005) and transferrin saturation (P = 0.0002) was seen in subjects with plasma retinol > or = 40 micrograms/dl, while subjects with plasma retinol < 20 micrograms/dl showed no response. Serum ferritin improved most in the retinol categories < 40 micrograms/dl, suggesting that the absorption of iron was not impaired by marginal vitamin A status, but that it was rather the mobilisation of iron from stores that was affected. Changes in vitamin A status correlated positively and significantly with changes in serum iron (r = 0.37; P = 0.0001) transferrin saturation (r = 0.27; P = 0.004) and haemoglobin (r = 0.21; P = 0.03), but negatively with serum ferritin (r = -0.28; P = 0.003). The presence of marginal vitamin A deficiency in a community may limit the effectiveness of an iron intervention programme and vitamin A status should therefore also be considered when such programmes are planned.
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PMID:Response to an iron fortification programme in relation to vitamin A status in 6-12-year-old school children. 909 48

A case-control study of 712 Brazilian mother-baby pairs was performed to assess maternal nutritional factors, more specifically low or marginal concentrations of vitamin A, folate and iron, as risk factors for intrauterine growth retardation (IUGR). Newborns were classified as being IUGR according to the Lubchenco classification. The gestational age of the newborns was evaluated by the Capurro method. Vitamin A, folate, ferritin and haemoglobin were measured by high-performance liquid chromatography, radioimmunoassay, immunoenzymetric assay and by the cyanmethaemoglobin method respectively. The relationship between maternal nutritional status and IUGR was investigated using stratification and logistic regression. According to the final logistic regression model, the risk factors for IUGR were: maternal body weight, per capita income, cigarette smoking, maternal weight gain, prior history of low birthweight, high maternal ferritin, beer intake and coffee intake. Specific interventions likely to have the major short-term impact in this region are not directly related to nutritional factors, but to efforts to reduce or eliminate toxic exposures. Over the long term, improvement in maternal nutritional status and socioeconomic conditions would be expected to produce important benefits.
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PMID:The influence of maternal nutritional factors on intrauterine growth retardation in Brazil. 913 8

Different supplementation schemes to build iron stores in female Indonesian adolescents were investigated. Subjects were 273 high-school girls allocated randomly to four treatment groups. During a 3-mo period one group received 60 mg Fe, 750 micrograms retinol, 250 micrograms folic acid, and 60 mg vitamin C per day; a second group received 60 mg Fe, 6000 micrograms retinol, 500 mg folic acid, and 60 mg vitamin C once a week; a third group received 120 mg Fe and the same amount of the other three micronutrients as the second group once a week; and a fourth group received only placebos. All subjects were dewormed and supplement allocation was double blind. Blood samples were collected at baseline, after 2 and 3 mo of supplementation, and 6 mo after the last supplement. After 2 mo of supplementation, groups supplemented weekly and daily showed similar significant improvements (P < 0.001) in hemoglobin and retinol concentrations, and supplementation for 3 instead of 2 mo did not significantly increase these two indicators. After 3 mo, the increase in ferritin was approximately equal to 27 micrograms/L in the daily and 14-15 micrograms/L in the weekly groups (P < 0.001), the latter having a final concentration of 42-45 micrograms/L. At 6 mo postsupplementation there were no significant differences among daily and weekly groups, but the ferritin concentration was still approximately equal to 10-12-micrograms/L higher (P < 0.001) than in the placebo group. The group supplemented weekly with 60 mg Fe complained less about side effects than the other supplemented groups (P < 0.05). Weekly supplementation with 60 mg Fe and 6000 micrograms retinol for 3 mo was optimal for improving the iron status of the adolescents for approximately equal to 9 mo.
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PMID:Weekly micronutrient supplementation to build iron stores in female Indonesian adolescents. 920 87

One hundred two normal healthy males and females were given 0, 8, 20 or 32 g/d olestra to which had been added graded amounts of vitamins A, D and E for 8 wk in a parallel, double-blind study. The primary purpose of the study was to determine the amounts of vitamins D and E needed to offset the effect of olestra on the availability of these vitamins. Serum concentrations of retinol, carotenoids, 25-hydroxyvitamin D metabolites, alpha-tocopherol, phylloquinone, lipids, ferritin and total iron, iron-binding capacity and hematology parameters, plasma concentrations of des-gamma-carboxyprothrombin and prothrombin, and urinary gamma-carboxyglutamic acid (Gla) excretion were measured biweekly. Clinical chemistry and urinalysis parameters, vitamin B12 absorption, and serum 1,25-dihydroxyvitamin D concentration were measured at wk 0 and 8. Serum concentrations of alpha-tocopherol and 25-hydroxyergocalciferol were restored to control concentration by adding 2.1 mg d-alpha-tocopheryl acetate and 0.06 microg ergocalciferol per gram of olestra, respectively, to the diet. Olestra reduced serum concentrations of 25-hydroxyergocalciferol, carotenoids and phylloquinone in a dose-responsive manner but did not affect Gla excretion, plasma des-gamma-carboxyprothrombin and prothrombin concentrations, overall vitamin D status, vitamin B12 absorption or iron status. Laboratory evaluations showed no olestra-related effects. Subjects in all groups reported mild to moderately severe transient gastrointestinal symptoms. These symptoms did not affect study compliance or the integrity of the data.
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PMID:Olestra's effect on vitamins D and E in humans can be offset by increasing dietary levels of these vitamins. 923 62

In Morocco, malnutrition is a public health problem. Indeed, 25% of 6- to 60-month-old children suffer from malnutrition. Imbalance between antioxidant protection and prooxidant stress has been reported to accurately predict the survival of malnourished children. Therefore, we determined blood antioxidant vitamins (retinol, alpha-tocopherol and carotenoids), trace elements (serum zinc, copper and selenium) and enzymes (erythrocyte Se glutathione peroxydase and Cu-Zn superoxide dismutase) as well as blood oxidative stress index [ferritine, thiobarbituric-acid reactants (TBARS)] in 21 children suffering from severe malnutrition, 15 children suffering from mild malnutrition and in 20 healthy control children. Selenium, retionol, alpha-tocopherol and carotenoids were significantly decreased in malnourished children. These decreases were related to the severity of malnutrition. Moreover, the percentage of vitamin and trace element concentrations under deficient cutoff were high in malnourished children. On the contrary, TBARS, ferritin and prognostic inflammatory and nutritional index (PINI) were significantly increased in malnourished children. Except for TBARS, these increases were related to the severity of malnutrition. On the other hand, blood retional, alpha-tocopherol, beta-carotene and selenium were negatively related to alpha 1-acid glycoprotein. Blood beta-cryptoxanthin, lycopene, carotenes and copper were positively related to weight. Finally, blood lutein/zeaxanthin and copper were positively related to height. These results confirm the imbalance between antioxidant protective factors and oxidative stress index in malnourished children. Moreover, the decrease in antioxidant protective factors is related to inflammation or stature. These results suggest that antioxidant micronutrient supplementation of the refeeding diet could be required in the nutritional rehabilitation of malnourished children.
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PMID:[Evaluation of oxidative stress and antioxidant defences in malnourished Moroccan children]. 932 20

Utilization of mRNAs containing iron-responsive elements (IREs) is modulated by iron-regulated RNA-binding proteins (iron regulatory proteins). We examine herein whether iron differentially affects translation of ferritin and mitochondrial aconitase (m-Acon) mRNAs because they contain a similar but not identical IRE in their 5'-untranslated regions. First, we demonstrate that m-Acon synthesis is iron-regulated in mammalian cells. In HL-60 cells, hemin (an iron source) stimulated m-Acon synthesis 3-fold after 4 h compared with cells treated with an iron chelator (Desferal). Furthermore, hemin stimulated m-Acon synthesis 2-4-fold in several cell lines. Second, we show that iron modulates the polysomal association of m-Acon mRNA. We observed m-Acon mRNA in both ribonucleoprotein and polyribosomal fractions of HL-60 cells. Hemin significantly increased the polyribosomal association and decreased the ribonucleoprotein abundance of m-Acon mRNA in HL-60 cells. Third, our results indicate that iron differentially regulates translation of m-Acon and ferritin mRNAs. A dose response to hemin in HL-60 cells elicited a 2-2.4-fold increase in m-Acon synthesis within 5 h compared with untreated cells, whereas ferritin synthesis was stimulated 20-100-fold. We conclude that iron modulates m-Acon synthesis at the translational level and that iron regulatory proteins appear to differentially affect translation of IRE-containing mRNAs.
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PMID:Iron differentially stimulates translation of mitochondrial aconitase and ferritin mRNAs in mammalian cells. Implications for iron regulatory proteins as regulators of mitochondrial citrate utilization. 945 6

Iron regulatory protein 1 (IRP1) and IRP2 are cytoplasmic RNA binding proteins that are central regulators of mammalian iron homeostasis. We investigated the time-dependent effect of dietary iron deficiency on liver IRP activity in relation to the abundance of ferritin and the iron-sulfur protein mitochondrial aconitase (m-acon), which are targets of IRP action. Rats were fed a diet containing 2 or 34 mg iron/kg diet for 1-28 d. Liver IRP activity increased rapidly in rats fed the iron-deficient diet with IRP1 stimulated by d 1 and IRP2 by d 2. The maximal activation of IRP2 was five-fold (d 7) and three-fold (d 4) for IRP1. By d 4, liver ferritin subunits were undetectable and m-acon abundance eventually fell by 50% (P < 0.05) in iron-deficient rats. m-Acon abundance declined most rapidly from d 1 to 11 and in a manner that was suggestive of a cause and effect type of relationship between IRP activity and m-acon abundance. In liver, iron deficiency did not decrease the activity of cytosolic aconitase, catalase or complex I of the electron transport chain nor was there an effect on the maximal rate of mitochondrial oxygen consumption with the use of malate and pyruvate as substrates. Thus, the decline in m-acon abundance in iron deficiency is not reflective of a global decrease in liver iron-sulfur proteins nor does it appear to limit ATP production. Our results suggest a novel role for m-acon in cellular iron metabolism. We conclude that, in liver, iron deficiency preferentially affects the activities of IRPs and the targets of IRP action.
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PMID:Dietary iron intake rapidly influences iron regulatory proteins, ferritin subunits and mitochondrial aconitase in rat liver. 948 59

To assess the nutritional status of 80 elderly living in a geriatric home, a cross-sectional study was designed. 40 men (76.1 +/- 8.2 years) and 40 women (83.1 +/- 6.9 years) were randomly selected. Anthropometric indicators (weight (W), height (H), triceps skinfold (TSF), muscle area (MA), fat area (FA), mid-arm circumference (MAC), arm muscle circumference (AMC) and body mass index (BMI)), biochemical parameters (hemoglobin, ferritin, cholesterol, albumin, zinc and vitamin A) and dietary intake (weighed method) were determined. MAC and AMC in men and PT and FA in women were below 10th percentile. 35.3% did not show signs of undernutrition, 39.7% was at nutritional risk (1 sign) and the other 25% was undernourished (2 or more signs). 8% showed anemia 52% had low values of ferritin, 13% were hypozincemic, 8% had vitamin A deficiency, 29% had hypoalbuminemia and 7.9% hipocholesterolemia. 50% and 48% of men and women had energy intake below 1.5 x BMR (n = 47). Vitamin A, C and zinc adecuacies were below 2/3 RDA. Evidence of the high nutritional risk of this elderly group is provided by alteration of anthropometric, biochemical and dietary indicators. Some other parameters must be assessed (reduced appetite, lack of foods) in order to detect more subtle changes of the nutritional status, and a nutritional intervention should be started immediately.
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PMID:[Nutritional status of institutionalized elderly. Valencia, State of Carabobo, Venezuela]. 983 Apr 84

Twenty-seven infants with classical phenylketonuria were evaluated longitudinally for 6 mo while ingesting Phenex-1 Amino Acid Modified Medical Food With Iron as their primary protein source. Intake of selected nutrients and biochemical indices of trace and ultratrace mineral status and plasma retinol and alpha-tocopherol concentrations were evaluated. The means of iron status indices (complete blood count, plasma ferritin, iron, transferrin saturation, total iron binding capacity) and the plasma concentrations of trace and ultratrace minerals (copper, manganese, molybdenum, selenium, zinc) and plasma retinol and alpha-tocopherol were in the reference ranges. Vitamin A intakes (r = 0.49, p < 0.05) and plasma retinol-binding protein concentrations (r = 0.42, p < 0.05) were positively correlated with plasma retinol concentrations at 3 mo of study. At 6 mo, concentrations of plasma transthyretin (r = 0.72, p < 0.01) and retinol-binding protein (r = 0.48, p < 0.05) were positively correlated with plasma retinol concentrations. At 6 mo, concentrations of plasma transthyretin (r = 0.52, p < 0.05) were positively correlated with retinol-binding protein concentrations. Phenex-1 supports normal mean iron status indices and mean concentrations of trace and ultratrace minerals, retinol, and alpha-tocopherol when fed in adequate amounts.
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PMID:Plasma micronutrient concentrations in infants undergoing therapy for phenylketonuria. 1006


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