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PubMed1996

The pH Requirement for in Vivo Activity of the Iron-Deficiency-Induced "Turbo" Ferric Chelate Reductase (A Comparison of the Iron-Deficiency-Induced Iron Reductase Activities of Intact Plants and Isolated Plasma Membrane Fractions in Sugar Beet).

The characteristics of the Fe reduction mechanisms induced by Fe deficiency have been studied in intact plants of Beta vulgaris and in purified plasma membrane vesicles from the same plants. In Fe-deficient plants the in vivo Fe(III)-ethylenediaminetetraacetic complex [Fe(III)-EDTA] reductase activity increased over the control values 10 to 20 times when assayed at a pH of 6.0 or below ("turbo" reductase) but increased only 2 to 4 times when assayed at a pH of 6.5 or above. The Fe(III)-EDTA reductase activity of root plasma membrane preparations increased 2 and 3.5 times over the controls, irrespective of the assay pH. The Km for Fe(III)-EDTA of the in vivo ferric chelate reductase in Fe-deficient plants was approximately 510 and 240 [mu]M in the pH ranges 4.5 to 6.0 and 6.5 to 8.0, respectively. The Km for Fe(III)-EDTA of the ferric chelate reductase in intact control plants and in plasma membrane preparations isolated from Fe-deficient and control plants was approximately 200 to 240 [mu]M. Therefore, the turbo ferric chelate reductase activity of Fe-deficient plants at low pH appears to be different from the constitutive ferric chelate reductase.

Journal Article↗
PubMed2001

Reduced thymocyte proliferation but not increased apoptosis as a possible cause of thymus atrophy in iron-deficient mice.

Iron deficiency induces thymus atrophy in laboratory animals and very likely in humans by unknown mechanisms. The atrophy is associated with impaired cell-mediated immunity. In this study, we tested the hypothesis that thymus atrophy is a result of increased apoptosis and reduced thymocyte proliferation. Thymocytes were obtained from twenty-seven control, twenty-seven pairfed, twenty-seven iron-deficient (ID) mice; twelve and fourteen ID mice that received the control diet (0.9 mmol/kg versus 0.09 mmol/kg for the ID diet) for 1 d (repletion, R1) and 3 d (R3), respectively. Cell cycle analysis and apoptosis were studied by flow cytometry using propidium iodide staining and terminal deoxyuridine nick end labeling of DNA breaks assay respectively. When mice were killed, haemoglobin, haematocrit, and liver iron stores of ID, R1, and R3 mice were 25-40 % of those of control and pairfed mice Absolute and relative thymus weights and thymocyte numbers were 19 to 68 % lower in ID, R1, and R3 than in control and pairfed groups We found no significant difference among groups in the percentage of cells undergoing apoptosis. A higher percentage of thymocytes from ID and R1 mice than those of control, pairfed, and R3 mice were in the resting phase of the normal cell cycle Conversely, a lower percentage of thymocytes from ID and R1 mice than those from control, pairfed, and R3 mice were in the DNA synthesis phase and late phase of DNA synthesis and onset of mitosis (G2-M) Indicators of iron status positively correlated (r 0.3 to 0.56) with the percentage of thymocytes in the G2-M phase Results suggest that reduced cell proliferation but not increased apoptosis is the cause of thymus atrophy associated with iron deficiency.

Anemia, Iron-Deficiency↗
PubMed1977

Iron-deficiency anaemia in pregnancy: (biochemical investigations of iron-deficiency and nutritional status).

Biochemical investigations on iron deficiency and nutritional status were carried out in a group of 130 women in the second or third trimesters of pregnancy and in 42 control non-pregnant women. The important findings were: 1. Anaemia was present in 46.1% of pregnant women in comparison with 19% in non-pregnant women. It was found to be more prevalent in the third trimester of pregnancy. 2. Iron deficiency with and without anaemia, as judged from serum transferrin saturation (%) was evident in 59.2% of pregnant women with an incidence of 70.3% in the third trimester of pregnancy. 3. Serum albumin, gamma globulin and A/G ratio were found to be decreased in pregnancy whereas serum levels of alpha-2 and beta globulins were elevated. The results have been discussed.

Adult↗
PubMed1988

Amylophagia and iron deficiency anemia.

Iron deficiency anemia may be associated with dietary practices such as amylophagia, which is seen frequently in women of certain ethnic origins. Starch eating may be a direct or indirect cause or symptom of iron deficiency anemia. Orofacial symptoms of amylophagia and iron deficiency anemia are discussed. A case in which anemia and dietary aberration were incidental to the admitting diagnosis is presented.

Adolescent↗
PubMed1990

Iron absorption in the iron-deficient rat.

Iron absorption in the iron-deficient rat was compared with that in the normal rat to better understand the regulation of this dynamic process. It was found that: Iron uptake by the iron-deficient intestinal mucosa was prolonged as a result of slower gastric release, particularly when larger doses of iron were employed. The increased mucosal uptake of ionized iron was not the result of increased adsorption, but instead appeared related to a metabolically active uptake process, whereas the increased mucosal uptake of transferrin iron was associated with increased numbers of mucosal cell membrane transferrin receptors. Mucosal ferritin acted as an iron storage protein, but its iron uptake did not explain the lower iron absorption in the normal rat. Iron loading the mucosal cell (by presenting a large iron dose to the intestinal lumen) decreased absorption for 3 to 4 days. Iron loading of the mucosal cell from circulating plasma transferrin was proportionate to the plasma iron concentration. Mucosal iron content was the composite of iron loading from the lumen and loading from plasma transferrin versus release of iron into the body. These studies imply that an enhanced uptake-throughout mechanism causes the increased iron absorption in the iron-deficient rat. Results were consistent with the existence of a regulating mechanism for iron absorption that responds to change in mucosal cell iron, which is best reflected by mucosal ferritin.

Anemia, Hypochromic↗
PubMedDate not supplied

Correction of iron deficiency with an iron-fortified fluid whole cow's milk in children: results of a pilot study.

PURPOSE: This study assesses the efficacy of an iron-fortified (15 mg Fe, as stabilized ferrous sulfate (SFE-171), per liter) fluid whole cow's milk (IFFWCM) for the treatment of mild iron deficiency in children. Previous studies in healthy adult volunteers showed a mean 10.2 +/- 4.7% iron absorption. PATIENTS AND METHODS: Seventeen children (12 to 48 months old) with iron deficiency (serum iron (SI) < 60 micrograms/dl, transferrin saturation (TS) < 15%, serum ferritin (SF) < 15 ng/ml) were included in this study; 11 of them were anemic. As treatment, they received IFFWCM, instead of the customary whole cow's milk, for at least 4 months; medicinal iron was not administered. Hematocrit (Hct), hemoglobin (Hb), SI, TS, and SF were determined monthly. RESULTS: The Hb increased from 10.3 +/- 0.8 to 12.7 +/- 0.6 g/dl in the group with anemia (delta F-B: 2.4 +/- 1.0 g/dl) and from 12.6 +/- 0.7 to 13.5 +/- 0.3 g/dl in the group without anemia (delta F-B: 0.9 +/- 0.5 g/dl); the difference between both groups was significant (p < 0.01); the rate for Hct values showed a similar pattern. In the whole group, the SI increased to 84.8 +/- 37.4 micrograms/dl, with no difference between children with anemia and children without anemia; TS showed a similar pattern (delta F-B: 19.0 +/- 11.0%). The mean SF increased from 12.1 +/- 2.7 ng/ml to 27.9 +/- 25.4 ng/ml. Normal values for Hct, Hb, SI, and TS were reached by 100% of children; the rate for SF was 56.3%. Time required to reach normal Hct in the children with anemia was 59.4 +/- 33.0 days. Acceptance and tolerance were excellent; no treatment had to be discontinued. The group of patients with anemia was compared with an historical group composed of 55 children matched for age, basal Hct, and achieved Hct increase, treated with medicinal FS (4-6 mg/kg/day): time required to reach normal Hct was shorter in the FS-treated group (39.0 +/- 14.5 days) (p = 0.050). CONCLUSION: The use of IFFWCM alone could be an effective, relatively inexpensive, and well-tolerated treatment of iron deficiency in children.

Anemia, Iron-Deficiency↗
PubMed2006

Erythrocyte CuZn superoxide dismutase activity is decreased in iron-deficiency anemia.

Iron and copper are essential microminerals that are intimately related. The present study was performed to determine the effect of iron-deficiency anemia (IDA) and treatment with iron on laboratory indicators of copper status. Hemoglobin, mean corpuscular volume erythrocyte Zn protoporphyrin, serum ferritin, serum copper, serum ceruloplasmin, and erythrocyte CuZn-superoxide dismutase (SOD) activity were studied in 12 adult women with IDA before and after iron treatment for 60-90 d (100 mg/d Fe, as ferric polymaltose) and in 27 women with normal iron status. Prior to treatment with iron, serum copper and ceruloplasmin were not different between the groups and treatment with iron did not affect these measures. IDA women, before and after treatment with iron, presented a 2.9- and 2-fold decrease in erythrocyte CuZn-SOD activity compared to women with normal iron status (p < 0.001). Treatment with iron increased erythrocyte CuZn-SOD activity of the IDA group; however, this change was not statistically significant. In conclusion, CuZn-SOD activity is decreased in IDA. Measurement of this enzyme activity is not useful for evaluating copper nutrition in iron-deficient subjects.

Adult↗
PubMed1987

Substrate-dependent functional defects and altered mitochondrial respiratory capacity in hearts from guinea pigs with iron deficiency anemia.

Iron deficiency anemia was induced by dietary means in weanling guinea pigs. A 25% higher ventricular wall mass per 100 g body mass was seen after 6 weeks of feeding. Myocardial performance was determined in isolated perfused hearts using an isovolumic Langendorff preparation. All hearts exhibited a 25% decrease in left ventricular developed pressure (LVDP) and decreased dP/dt when substrate was switched from 10 mM pyruvate to 16.6 mM glucose. The glucose reduction in LVDP resulted from decreased systolic pressure, which completely reversed when hearts again metabolized pyruvate. With glucose as substrate, left ventricular developed pressure-end diastolic volume relationships were indistinguishable. However, with pyruvate, iron-deficient hearts appeared to be less responsive to the increased energy demands required by elevated diastolic volumes. Rates of state 3 respiration were 18% below control with glutamate + malate as substrate, and 38% lower with pyruvate + malate in mitochondria isolated from anemic animals. No differences in respiration were noted with succinate. Cytochrome a + a3 content, cytochrome oxidase activity and total mitochondrial protein content appeared to be unchanged. In contrast, cytochromes b, c + c1, and the flavoproteins were significantly decreased. The data suggest that iron deficiency anemia induces cardiac hypertrophy with a fixed but defective mitochondrial population, potentially placing the heart in an energetic imbalance. These differences in mitochondrial function were expressed by decreased myocardial performance when the heart metabolizes pyruvate, an exclusively aerobic substrate.

Anemia, Hypochromic↗
PubMed1996

Effect of iron-supplemented total parenteral nutrition in patients with iron deficiency anemia.

Iron deficiency anemia is common among hospitalized patients, and blood losses from diagnostic phlebotomy increase the likelihood of a negative iron balance. The role for iron supplementation of total parenteral nutrition (TPN) in these patients is unclear. Twenty-three patients with iron deficiency anemia were identified. Twelve patients were randomized to receive TPN without iron (group 1) and 11 received TPN supplemented with 10 mg of iron as iron dextran daily (group 2). Both groups were matched for age, serum iron studies, red cell indices, and hemogram. After a 7-d period, the mean serum iron in group 2 increased from 10 to 26 micrograms/dL, with an increased transferrin saturation from 7.3 to 15.3% (each, p < 0.05). No changes in total iron binding capacity, ferritin, reticulocyte count, hemoglobin, hematocrit, or mean corpuscular volume were observed in the two groups. The incidence of infectious complications was not different between both groups. We conclude that iron supplementation of TPN appears safe and is effective in increasing serum iron levels. The use of iron-supplemented short-term TPN needs to be further studied given no change in red cell indices, hemoglobin, hematocrit, or transfusion requirement.

Adult↗
PubMed2002

Twenty-four-hour motor activity in human infants with and without iron deficiency anemia.

Iron deficiency anemia (IDA) is a very common nutritional problem that alters motor activity. The aim of this study was to compare 24-h motor activity in the home in healthy 6-month-old infants with and without IDA. Activity was assessed via actigraphs on the leg during 24 continuous hours in 17 Chilean infants with IDA and 18 with normal hemoglobin levels. All infants were given oral iron, and activity was reassessed at 12 and 18 months. The frequency of movement units per minute was determined for each waking/sleep state during the day and night, and the duration of each state was computed. At 6 months of age, there were no differences between anemic and nonanemic infants in time per state. However, infants with IDA showed an overall increase in motor activity compared to controls. These differences were no longer observed at 12 and 18 months of age. Increased activity during the period of IDA raises the issue of a shared underlying mechanism with restless legs syndrome, a sensorimotor dysfunction where iron deficiency increases the severity of the symptoms and iron supplementation ameliorates them. Due to previous findings of decreased motor activity in the laboratory at 12 months during the waking time surrounding an afternoon nap, we also compared those data to a nap in the home. Infants with IDA were less active in the laboratory than in the home. The home versus laboratory results suggest that contextual factors affect the motor activity of IDA infants to a larger extent than controls.

Anemia, Iron-Deficiency↗
PubMed2004

Plasma selenium status in children with iron deficiency anemia.

Iron and selenium are trace elements necessary for the maintenance of life and health. Iron deficiency is the most common nutritional deficiency among children in the world. The purpose of this study was to evaluate plasma selenium concentrations in children with iron deficiency anemia (IDA). Plasma selenium levels were investigated in 56 children with IDA and in 48 control subjects aged 1-8 years. A spectrofluorometric method was used for the determination. Plasma selenium concentrations in children with IDA (33.6+/-8.2 microg/l) were significantly lower than in the control group (56.0+/-17.0 microg/l) (p<0.001). However, there was no relation between plasma selenium, iron and hemoglobin concentrations.

Anemia, Iron-Deficiency↗
PubMed1979

[Serum ferritin and cytochemical storage iron in erythropoiesis and the R.E.S. in iron deficiency and faulty iron metabolism].

In 60 patients with iron deficiency anemia of chronic disorders serum iron, an iron absorption test, serum transferrin, serumferritin and stainable non-heme iron in erythropoiesis and reticuloendothelial system, were evaluated. Intercorrelations of these parameters were studied in different diagnostic groups. Pathogenetic principles and the clinical value of the applied diagnostic methods are discussed.

Adult↗
PubMedDate not supplied

Incidence of iron-deficiency anaemia and depleted iron stores among nine-month-old infants in Vancouver, Canada.

The iron status and feeding practices of 434 infants in Vancouver were determined at 39 +/- 1 week of age. Iron-deficiency anaemia (haemoglobin < or = 101 g/L, or < or = 110 g/L with two or three abnormal results from tests of serum ferritin, zinc erythrocyte protoporphyrin and total iron binding capacity) occurred in 7% of infants. Low iron stores (serum ferritin < 10 micrograms/l) occurred in about 24% of infants. Iron-deficiency anaemia was significantly associated (p < 0.001) with duration of breastfeeding. The prevalence of iron-deficiency anaemia among infants breastfed for 8 months was 15%. At 39 weeks (9 months) of age, about 5% and 13% of the infants were bottle-fed with cows milk or low iron infant formula, respectively, and this was also significantly associated (p < 0.02) with low iron stores. Iron-fortified infant cereals had been introduced to 95% of the infants by six months of age. This study shows iron-deficiency anaemia is a problem among a significant number of nine-month-old infants in Canada, and is not explained by failure to introduce iron-fortified infant cereals.

Anemia, Iron-Deficiency↗
PubMed1980

[Therapy of juvenile iron deficiency with bivalent iron dragees (Fe2-fumarate, succinate, sulfate). Controlled double-blind study].

In 53 children with moderate iron deficiency (haemoglobin 7,5 to 12 g/dl) divalent iron salts as tablets (59Fe2+-fumarate, -succinate, -sulfate) were tested versus placebo (controlled double-blind study). Gastrointestinal side effects were most frequently seen with iron succinate (50%) and iron sulfate (25%). Therapeutic success as measured by haemoglobin regeneration was not significantly different among the three iron salts, but significantly more effective than in the placebo group. Children beyond the age of two years mostly refused the application of tablets and should be supplied with liquid preparations.

Anemia, Hypochromic↗