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

Ascorbate is an important cofactor in many cellular metabolic reactions and is intimately linked to iron homeostasis. Continuously cultured cells are ascorbate deficient due to the lability of the vitamin in solution and to the fact that daily supplementation of media with ascorbate is unusual. We found that ascorbate repletion alone did not alter ferritin synthesis. However, ascorbate-replete human hepatoma cells, Hep3B and HepG2, as well as K562 human leukemia cells achieved a substantially higher cellular ferritin content in response to a challenge with iron than did their ascorbate-deficient counterparts grown under standard culture conditions. Most of the elevation in ferritin content was due to an increase in de novo ferritin synthesis of greater than 50-fold, as shown by in vivo labeling with [35S]methionine and immunoprecipitation. RNA-blot analysis showed only minor changes in steady state levels of ferritin mRNA, suggesting that ascorbate enhances iron-induced ferritin synthesis primarily by post-transcriptional events. Transient gene expression experiments using chloramphenicol acetyltransferase reporter gene constructs showed that the ascorbate effect on ferritin translation is not mediated through the stem-loop near the translational start site that transduces ferritin synthesis in response to cytokines. The data suggest that ascorbate possibly modifies the action of the iron-responsive element on ferritin translation, although more precise structure-function studies are needed to clarify this issue. These data demonstrate a novel role of ascorbate as a signaling molecule in post-transcriptional gene regulation. The mechanism by which ascorbate modulates cellular iron metabolism is complex and requires additional detailed investigation.
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PMID:Ascorbic acid enhances iron-induced ferritin translation in human leukemia and hepatoma cells. 785 59

Healthy individual were given 2 g of vitamin C per day for 2 months. Whole blood iron, ascorbic acid, hemoglobin, and serum ceruloplasmin were determined at the beginning, and 1 or 2 months after the start of the experiment. The concentration of ascorbic acid was observed to increase significantly in the blood, while blood iron, hemoglobin, and serum ceruloplasmin levels significantly increased at the end of the 1st month, but decreased to control levels at the end of the 2nd month. Male albino guinea pigs were administered 8, 180, and 360 mg of vitamin C per day for 2 months. Liver ferritin iron, liver copper, serum copper, and serum ceruloplasmin levels significantly decreased, but there was no significant change in hemosiderin iron while blood ascorbic acid significantly increased at the end of the 2 month period. There was no significant change in serum iron and hematocrit levels. These results suggest that vitamin C has an antagonistic effect on copper metabolism in guinea pigs but not in humans either on copper or iron metabolisms.
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PMID:Effect of vitamin C on copper and iron status in men and guinea pigs. 789 Dec 1

Caco-2 cells grown in bicameral chambers, a model of intestinal epithelial iron transport (Biochim. Biophys. Acta (1991) 1070, 205-208), were used to study the effect of apo-transferrin (apo-Tf) in the basal chamber on 59Fe uptake from the apical surface, intracellular 59Fe distribution, and 59Fe transport into the basal chamber. Caco-2 cells were grown with varying amounts of iron to achieve cells that were either iron-deficient (FeD), or normal iron status (FeN), or iron-loaded (FeH). The effect of apo-Tf was most marked in FeD cells with the transport of 59Fe from 1 microM 59Fe-ascorbate on the apical side to the basal chamber measured as (22.2 +/- 3.0) x 10(4), (8.2 +/- 0.6) x 10(4), and (2.7 +/- 0.4) x 10(4) atoms 59Fe/cell/min in the presence of apo-Tf, BSA, and no added protein, respectively. Unexpectedly in FeD cells total 59Fe uptake (i.e., both 59Fe in the cells and that transported into the basal chamber) was decreased by basolateral apo-Tf with total uptake of (2.6 +/- 0.3) x 10(5), (4.8 +/- 0.6) x 10(5), and (4.8 +/- 0.7) x 10(5) atoms/cell/min with apo-Tf, BSA, and no additions, respectively. Analysis of intracellular 59Fe by isoelectrofocusing in polyacrylamide gels demonstrated 59Fe migrating both with a basic pI and with the pI values of ferritin (Ft) at a ratio of 200:1 (basic pI moiety: ferritin) in FeD cells. The presence of Tf further decreased the small amount of 59Fe in Ft. These studies demonstrate that basolateral Tf affects the apical uptake of 59Fe, the intracellular distribution of 59Fe, and the transport of 59Fe across intestinal epithelium, the latter effect occurring even when cellular content of ferritin is high.
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PMID:Regulation of iron uptake and transport by transferrin in Caco-2 cells, an intestinal cell line. 801 2

This county-based correlation study examined associations of breast cancer mortality with dietary habits and certain serum biochemical markers, utilizing data collected from an ecological survey in 65 Chinese rural counties. Univariate correlation and multivariate regression analysis showed that consumption of animal foods, including eggs, fish and meat, was positively linked to county-wide mortality rates of breast cancer in Chinese women. No clear associations between breast cancer mortality rates and consumption of green vegetables, carrots and fruits were observed in this study. A modest inverse correlation between serum vitamin C levels and breast cancer mortality was observed, while selenium levels were positively related to the mortality rates. Positive correlations for serum ferritin and hemoglobin were found, in agreement with recent reports of an elevated cancer risk with increased body iron stores. Limitations of these ecological data preclude causal inferences, but the findings provide clues to breast cancer risk and protective factors in a low incidence area of the world.
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PMID:Diet, serum markers and breast cancer mortality in China. 806 9

Ascorbic acid at pharmacologically attainable concentrations effectively inhibited the growth of the catecholamine-positive neuroblastoma cell line SK-N-SH; it inhibited LS cells to a smaller extent and catecholamine-negative SK-N-LO cell growth least effectively. In all three cell lines high concentrations of H2O2 were found. Since ascorbic acid was shown to release iron from ferritin in vitro and to keep it in the reduced state, we suggested that it acted as a pro-oxidant in ferritin-rich neuroblastoma cells in the presence of H2O2 and Fe2+ (Fenton reaction), implying iron release from cellular ferritin. We show here that iron could be mobilized from cellular ferritin by 1 mM ascorbic acid in iron-59-preloaded SK-N-SH and LS cells, but not in SK-N-LO cells. In agreement with these results, DNA strand break formation by ascorbate was only observed in SK-N-SH and LS cells. In SK-N-LO cells, DNA strand breaks could be induced by a combination of 1 mM ascorbic acid and 100 microM H2O2. Since cell-damaging effects caused by chemotherapy further facilitate iron release from ferritin, we conclude that ascorbate could be a powerful enhancer of some cytostatic drugs in neuroblastoma therapy.
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PMID:Ascorbic-acid-mediated iron release from cellular ferritin and its relation to the formation of DNA strand breaks in neuroblastoma cells. 818 35

Effects of iron supplementation on growth and hematological status of Indonesian anemic preschool children with low weight-for-age were investigated. A treatment group (n = 39) received daily supplements of 30 mg Fe and 20 mg vitamin C, whereas a control group (n = 37) received 20 mg vitamin C only for a period of 2 mo. Supplement allocation was double blind. At the start and finish of the study, body weight, height, food intake, and hemoglobin and serum ferritin concentrations were determined. Only the treatment group showed a significant increase in all hematological values (P < 0.001). Height and weight of all children increased (P < 0.01). Increases in height and height-for-age Z score in the treatment group were larger (P = 0.001) than the increase in the control group. The positive effect of iron supplementation on linear growth was not caused by increased food intake, but seems to be influenced by decreased morbidity. Iron supplementation may be a relatively inexpensive way to help decrease the high prevalence of stunting.
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PMID:Decreased rate of stunting among anemic Indonesian preschool children through iron supplementation. 823 43

One hundred four infants were randomly assigned to receive whole cow milk plus iron-fortified cereal (WCM + C) in accord with the previous recommendations of the Committee of Nutrition/American Academy of Pediatrics (CON/AAP); one of two iron-fortified, follow-up formulas; or an iron-fortified infant formula. Mean iron intakes and vitamin C exceeded the recommended dietary allowance in all groups. By 12 mo of age, mean ferritin and mean corpuscular volume were lower in the WCM + C group and significantly more infants had serum ferritin concentrations < 12 micrograms/L. We conclude that infants 6-12 mo of age fed whole cow milk and iron-containing table food are at risk of developing depleted iron stores but not anemia. The iron insufficiency in these infants is not due to inadequate intake of iron or vitamin C, but probably to relatively poor bioavailability of iron in infant cereal.
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PMID:Iron status and intake of older infants fed formula vs cow milk with cereal. 823 44

The purpose of the study was to assess the prevalence of Fe deficiency and Fe-deficiency anaemia in a group of apparently healthy adolescents, and to assess the value of a food frequency and amount questionnaire as a screening tool to identify children at risk of Fe deficiency. White schoolchildren (399) aged 12-14 years living in a Southwest London suburb completed a food frequency and amount questionnaire to assess usual Fe and vitamin C intake, and provided a thumb-prick blood sample for analysis of haemoglobin (Hb), packed cell volume (PCV), and serum ferritin (SF). Children were classified as 'anaemic' if Hb was below the Dallman 3rd percentile (girls: < 120 g/l; boys: < 122, < 124 and < 126 g/l at ages 12, 13 and 14 years respectively); and 'low' or 'borderline' in Fe stores if SF was < 12 micrograms/l, or between 12 and 20 micrograms/l respectively. Of the boys and girls 3.5 and 10.5% respectively were anaemic; 1% of boys and 4% of girls had low ferritin values, and 14% of boys and 16% of girls were borderline. Fe intakes were significantly higher in boys than in girls (12.3 v. 9.6 mg/d, P < 0.001). Prevalence of anaemia was 14.5% in the group with both low Fe intakes (< lower reference nutrient intake) and low vitamin C intakes (< median), compared with 2.3% in the group with both high Fe intakes (> reference nutrient intake) and high vitamin C intakes (> median).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Haemoglobin, ferritin, and iron intakes in British children aged 12-14 years: a preliminary investigation. 839 96

To evaluate the relationship between cervical intraepithelial neoplasia (CIN) and undernutrition, a pair-matched case-control study was conducted in a low-income urban population. As a broad measure of nutritional status, serum albumin, serum ferritin, hematocrit, percent desirable weight, and percent calories consumed as protein were examined. Cases (n = 102) had biopsy-confirmed CIN I, II, or III, and clinic controls (n = 102), matched on age, race, and clinic, had normal Pap smears. Survey-collected data and frozen serum were utilized to study the hypothesized association. Crude and adjusted odds ratios and 95% confidence intervals were estimated using conditional logistic regressions. Results suggest a protective role for serum ferritin for those in the highest quartile relative to those in the lowest quartile. Controlling for smoking and monthly personal income, an adjusted odds ratio of 0.2 with a corresponding 95% confidence interval of 0.1-0.7 was observed. Similar findings were noted when all other available CIN risk factors were controlled. In addition, a dose gradient was present for dietary iron intake (p = 0.01). No associations were observed between each of the other undernutrition indexes and CIN. Although only high levels of serum ferritin were associated with a protective effect against CIN, when coupled with the results from other studies that suggest carotenoids, folates, and vitamin C to be protective, the overall hypothesis that poor nutriture is associated with CIN remains viable. Lack of an association with the other nutritional indexes may reflect the relatively sufficient nutritional status of low-income individuals residing in the United States, as opposed to the undernourished population of the Third World.
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PMID:Undernutrition as a risk factor for cervical intraepithelial neoplasia: a case-control analysis. 841 30

To examine the relationship between hepatic iron stores and plasma ferritin concentration in individuals treated with red cell transfusion and iron chelation therapy, 37 patients with sickle cell anemia and 74 patients with thalassemia major were studied. In each patient, hepatic iron stores were measured by an independently validated noninvasive magnetic method, and plasma ferritin was determined by immunoassay. The correlation between hepatic iron and plasma ferritin was significant both in patients with sickle cell anemia (R = 0.75, P < 0.0001) and in those with thalassemia major (R = 0.76, P < 0.0001). Regression analysis showed no significant difference between the two groups in the linear relationships between hepatic iron stores and plasma ferritin. Considering all 111 transfused patients as a group, the coefficient of correlation between hepatic iron stores and plasma ferritin was highly significant (R = 0.76, P < 0.0001). Regression analysis found that variation in body iron stores, as assessed by magnetic determinations of hepatic iron, accounted for only approximately 57% of the variation in plasma ferritin, suggesting that the remainder was the result of other factors, such as hemolysis, ineffective erythropoiesis, ascorbate deficiency, inflammation, and liver disease. The 95% prediction intervals for hepatic iron concentration, given the plasma ferritin, were so broad as to make a single determination of plasma ferritin an unreliable predictor of body iron stores. Variability resulting from factors other than iron status limits the clinical usefulness of the plasma ferritin concentration as a predictor of body iron stores.
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PMID:Hepatic iron stores and plasma ferritin concentration in patients with sickle cell anemia and thalassemia major. 841 2


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