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PubMed2002

Iron deficiency and iron excess damage mitochondria and mitochondrial DNA in rats.

Approximately two billion people, mainly women and children, are iron deficient. Two studies examined the effects of iron deficiency and supplementation on rats. In study 1, mitochondrial functional parameters and mitochondrial DNA (mtDNA) damage were assayed in iron-deficient (< or =5 microg/day) and iron-normal (800 microg/day) rats and in both groups after daily high-iron supplementation (8,000 microg/day) for 34 days. This dose is equivalent to the daily dose commonly given to iron-deficient humans. Iron-deficient rats had lower liver mitochondrial respiratory control ratios and increased levels of oxidants in polymorphonuclear-leukocytes, as assayed by dichlorofluorescein (P < 0.05). Rhodamine 123 fluorescence of polymorphonuclear-leukocytes also increased (P < 0.05). Lowered respiratory control ratios were found in daily high-iron-supplemented rats regardless of the previous iron status (P < 0.05). mtDNA damage was observed in both iron-deficient rats and rats receiving daily high-iron supplementation, compared with iron-normal rats (P < 0.05). Study 2 compared iron-deficient rats given high doses of iron (8,000 microg) either daily or every third day and found that rats given iron supplements every third day had less mtDNA damage on the second and third day after the last dose compared to daily high iron doses. Both inadequate and excessive iron (10 x nutritional need) cause significant mitochondrial malfunction. Although excess iron has been known to cause oxidative damage, the observation of oxidant-induced damage to mitochondria from iron deficiency has been unrecognized previously. Untreated iron deficiency, as well as excessive-iron supplementation, are deleterious and emphasize the importance of maintaining optimal iron intake.

Animals↗

PubMed1995

Iron deficiency and iron overload in Swedish male adolescents.

OBJECTIVES: The present study was undertaken to confirm or reject recent findings indicating a high prevalence of iron deficiency in Swedish male adolescents; a second aim was to study the prevalence of genetic iron overload. DESIGN: The diagnostic criteria were: anaemia: Hb < 130 g L-1 (a): iron deficiency: serum ferritin (SF) < 12 micrograms L-1 + transferrin saturation (TS) < 16% (b): iron deficiency anaemia a + b. Iron overload: SF (90th percentile) + TS (90th percentile) in repeat tests. SETTING: Central Sweden. SUBJECTS: A total 3975 men aged 18 years studied on enrollment into military service. RESULTS: Serum ferritin averaged 36.8 micrograms L-1. Anaemia was present in 0.5%, iron deficiency anaemia in 0.17% and iron deficiency in 0.4%. If iron deficiency is defined as SF < 16 micrograms L-1, as was recently suggested, the prevalence would be 2.8%. Such a cut-off value would include 73% normal people (false positives). Iron overload had the same prevalence as iron deficiency, 0.4%. CONCLUSIONS: Iron stores, as measured by serum ferritin, are small in young men studied at the end of their growth spurt. However, iron deficiency is rare. Therefore, the present study has not been able to confirm the high prevalence of iron deficiency recently reported. A prevalence of genetic haemochromatosis of 0.4%, confirms earlier findings and would mean that 12.6% of the population are heterozygotic carriers of the iron-loading genes. These findings give no support for a proposed, more effective iron-enrichment of food. It is not needed and can be harmful.

Adolescent↗

PubMed1992

Salivary iron status in children with iron deficiency and iron overload.

Forty anaemic (iron deficiency anaemia-27, thalassemia major-8, and aplastic anaemia-5) and 10 non-anaemic children (serving as controls) aged from 8 months to 10 years were selected for the study. The salivary iron was significantly higher in iron deficient and iron overload conditions compared to controls. The mean salivary:serum iron ratio was same in control and iron overload cases, while it was twice as high in iron deficient anaemic children. The correlation between salivary iron and serum iron was significant (r = 0.7392, P less than 0.001) in these cases. The iron deficient anaemic children with hypoalbuminaemia had significantly reduced serum and salivary protein (P less than 0.001), but iron concentrations in serum and saliva remained unaltered. The salivary protein level had significant correlations with serum albumin and serum protein (P less than 0.001). Thus, the iron in saliva is maintained at a higher level and more so in iron deficiency anaemia; it correlates well with serum iron (r = 0.6853, P less than 0.001) in iron deficient anaemic children also and is not affected by co-existing hypoproteinaemic situation.

Albumins↗

PubMed2003

Novel roles for iron regulatory proteins in the adaptive response to iron deficiency.

Iron regulatory proteins (IRP) modulate the use of mRNA-encoding proteins that are involved in the transport, storage and use of iron. Several new potential mRNA targets for IRP were recently identified: divalent metal transporter-1 (DMT-1) and ferroportin, which are critical regulators of iron absorption in the gut and of iron cycling between various tissues of the body. Although this may extend the reach of IRP to other processes that are important for maintaining body iron homeostasis, the extent to which IRP modulate other physiological processes that are altered in response to changes in iron availability is not clear. However, in the past several years, targets for IRP and IRP-like proteins were identified in eukaryotes and prokaryotes in the tricarboxylic acid (TCA) cycle and electron-transport chain. In mammals, this includes the mRNA that encodes the TCA-cycle enzyme mitochondrial aconitase (m-acon). Recent work established that m-acon expression is translationally regulated by iron in a manner that is strongly correlated with IRP RNA-binding activity. Interestingly, these studies also demonstrate that IRP regulate their mRNA targets in a hierarchical manner. The changes in m-acon synthesis and abundance in liver during iron deficiency fail to affect TCA-cycle capacity but are associated with a significant upregulation of mitochondrial export of radiolabeled citrate. We conclude that IRP are required for the regulation of physiological pathways that include but are not limited to iron metabolism, and as such, IRP are critical factors in the adaptive response to iron deficiency.

5' Untranslated Regions↗

PubMed1997

Technological approaches to combatting iron deficiency.

Iron deficiency is widespread among young children and women of reproductive age, especially in less industrialized countries. It is partly induced by plant-based diets containing low levels of poorly bioavailable iron. The most effective technological approaches to combat iron deficiency in less industrialized countries include supplementation targeted to high risk groups combined with a national program of food fortification and dietary strategies designed to maximize the bioavailability of both the fortificant and the intrinsic food iron. Prerequisites for effective supplementation include an efficient and consistent supply, delivery, and consumption of a highly bioavailable iron supplement. Fortification relies less heavily on compliance and an organized health service but must be regulated by government to eliminate competition with unfortified products. To be effective, a combination of an iron fortificant and food vehicle must be selected which is safe, acceptable to and consumed by the target population, does not adversely effect the organoleptic qualities and shelf-life of the food vehicle, and provides iron in a stable, highly bioavailable form. Bioavailability of both the fortificant and the intrinsic food iron can be improved by adding enhancing factors, removing inhibitors such as phytate by enzymatic and non-enzymatic hydrolysis, and using 'protected' fortification compounds.

Adult↗

PubMed1998

Effects of iron deficiency on iron distribution and gamma-aminobutyric acid (GABA) metabolism in young rat brain tissues.

Effects of iron deficiency on the distribution of iron and glutamate decarboxylase (GAD), gamma-aminobutyric acid transaminase (GABA-T) activities and GABA concentrations in different brain regions in young rats were investigated. Iron deficiency was induced by feeding an iron-depleted diet (0.32mg/100g) in weanling rats for 3 weeks or 6 weeks. The values of hemoglobin (Hb), hematocrit (Ht) and red blood cells (RBC) decreased with the progress of anemia. The concentrations of serum iron in the rats fed iron-depleted diets were lower than those of corresponding controls. On the other hand, the concentrations of total iron-binding capacity (TIBC) and unsaturated iron-binding capacity (UIBC) in serum were higher than those of corresponding controls. These results showed that hypochromic and typical iron-deficiency anemia had occurred in these rats. At the same time, iron deficiency also resulted in significantly low iron concentrations in the brain, especially in the hypothalamus, midbrain and thalamus, and striatum and hippocampus. Although the changes in GABA concentrations in corresponding brain regions were not observed, the activities of the GABA-synthesizing enzyme GAD and GABA-degrading enzyme GABA-T of the rats fed iron-depleted diets for 6 weeks decreased significantly. This study provides evidence that iron deficiency in the brain could change the utilization and metabolism of GABA.

4-Aminobutyrate Transaminase↗

PubMed1986

The liabilities of iron deficiency.

Iron has been recognized as a potent hematinic since the inception of hematology as a clinical discipline. Even ancient civilizations believed in the beneficial effects of medicinal iron. Nevertheless, the precise functional liabilities of iron lack remain the subject of continuing debate. The consequences of iron deficiency, particularly from a socioeconomic standpoint, are especially important in light of its high global prevalence. A recent review of the literature indicates that approximately 30% of the estimated world population of nearly 4.5 billion are anemic, and at least half of these, 500 to 600 million people, are believed to have iron deficiency anemia.

Adult↗

PubMed1983

Ferritin in the red cells of normal subjects and patients with iron deficiency and iron overload.

Red cell ferritin was measured in normal subjects and patients with iron deficiency and iron overload by means of radioimmunoassays with antibodies to liver (basic) and heart (acidic) ferritins. In most of the subjects examined, red cells were found to contain greater amounts of heart-type than liver-type ferritin. The basic ferritin content reflected the abnormal body iron status both in iron deficiency and iron overload while the acidic ferritin content was less closely related to the iron status. The two immunologically different red-cell ferritins probably represent distinct ferritin molecules and may have different metabolic functions within haem-synthesizing erythroid cells.

Anemia, Aplastic↗

PubMed1986

Cognitive deficits in iron-deficient and iron-deficient anemic children.

Eighteen- to 60-month-old iron-deficient anemic children given iron therapy (n = 25) and a control group matched for mother's educational level showed no significant difference in mean mental development score at baseline. The control group's mean score was increased significantly over baseline score at 3 and 6 months and was significantly higher than the experimental group's mean score at 3 months. Although the experimental group demonstrated hematologic correction over 6 months, mean mental development score showed no significant improvement. Scores for an iron deficient not anemic group given iron (n = 22), despite complete hematologic correction over the six months of observation, and for its control group, did not change significantly. Baseline scores for an iron-deficient not anemic placebo group (n = 23) and for its control group were not significantly different. At 3 months the control group score had increased significantly, whereas that for the experimental group had not. When experimental and control subjects were matched on baseline mental development score, the control subjects experienced increases in scores over time, further confirming an impaired ability to improve scores with repeated testing in the experimental groups. Behavioral rating data (responsiveness to examiner, responsiveness to environment, and emotional tone) revealed significant differences between the iron-deficient anemic group and its control group at 3 and 6 months, with the control group rated more responsive, suggesting that iron deficiency, alone or in association with anemia, may have some lasting effect on behavior and development. Group differences were also found between the mean number of occurrences of multiple stressful events. Failure to show improvement in scores in the iron-deficient anemic group may reflect the fact that those children were less testable than were children in the control group, despite repeated testings, a theory supported by the infant behavior rating data. This may be related to some irreversible behavioral deficit or to an adverse environmental milieu (e.g., stress).

Anemia, Hypochromic↗

PubMed2000

Iron status in Danes 1994. II: Prevalence of iron deficiency and iron overload in 1319 Danish women aged 40-70 years. Influence of blood donation, alcohol intake and iron supplementation.

Iron status, i.e. serum ferritin and haemoglobin (Hb) levels, was assessed in a population survey in 1994 (Dan-Monica 10) comprising 1319 Caucasian Danish women in age cohorts of 40, 50, 60 and 70 years. In the entire series, ferritin levels increased significantly from 40 years to 60 years of age. The prevalence of small iron stores (ferritin 16-32 microg/l), depleted iron stores (ferritin < 16 microg/l) and of iron deficiency anaemia (ferritin < 13 microg/l and Hb < 121 g/l) decreased steadily with age. Blood donors (n = 109) had lower ferritin levels than non-donors (P<0.0001). Ferritin levels in donors were inversely correlated with the cumulated number of lifetime phlebotomies (r(s) = -0.25, P<0.01). Ferritin levels in non-donors (n = 1208) were low in 40-year-old women (median 40 microg/l) and increased to a median of 95 microg/l in 60- and 70-year-old women (P<0.0001). In non-donors 40 years of age, the prevalence of small iron stores was 40.4%, the prevalence of depleted iron stores 10.8% and the prevalence of iron deficiency anaemia 2.16%. The prevalence of iron overload (ferritin >300 microg/l) was 1.54%. Ferritin levels in 60- and 70-year-old non-donors were correlated with the body mass index (r(s) =0.11, P=0.01). Ferritin levels in 50- to 60-year-old non-donors were correlated with alcohol intake (r(s)=0.23, P<0.0001). In the entire series, 37.5% of non-donors took supplemental ferrous iron (median 14 mg iron per day). Iron supplements had a significant positive influence on iron status in 40-year-old premenopausal non-donors but no effect in postmenopausal women or in donors. Non-donors (n = 170) treated with acetylsalicylic acid had lower ferritin levels (median 55 microg/l) than non-treated (n = 1038; median 75 microg/l) (P<0.0001). Compared with the Dan-Monica 1 iron status survey in 1984, the prevalence of iron deficiency and iron deficiency anaemia was unchanged, whereas the prevalence of iron overload displayed a slight increase. The 1987 abolition of the mandatory iron fortification of flour apparently had no negative effect on iron status.

Adult↗

PubMed1998

[The frequency and development of tissue iron deficiency in 6 iron deficiency anemia patients with plummer-vinson syndrome].

The physical signs of tissue iron deficiency include smooth and red tongue, angular stomatitis, koilonychia, and pica. The incidence of these conditions is unknown in Japan. We evaluated the frequency and development of tissue iron deficiency in 353 patients with iron deficiency anemia. The frequency of tissue iron deficiency was 6.8%; papillary atrophy of the tongue, 5.4%; abnormal nails, 5.4%; angular stomatitis, 1.1%; Plummer-Vinson syndrome, 1.7%; and pica, 0.06%. These findings were compared with the date collected by Wintrobe and Beveridge. The development and incidence of tissue iron deficiency correlated significantly with the severity of iron deficiency anemia.

Adult↗

PubMed1997

Regional brain iron, ferritin and transferrin concentrations during iron deficiency and iron repletion in developing rats.

Iron deficiency in young rats leads to a decrease in brain iron and ferritin concentrations, an increase in transferrin (Tf) concentration, and an increased rate of uptake of iron from the plasma pool. We conducted two experiments to determine whether brain iron, Tf and ferritin respond quickly to iron repletion and to determine whether brain regions respond heterogeneously. Weanling male Sprague-Dawley rats were fed an iron-deficient diet (<5 mg/kg Fe) for 2 wk followed by an iron-adequate diet (REPL group, 35 mg/kg Fe in Experiment 1 and 15 mg/kg Fe in Experiment 2) for 2 or 4 wks, respectively. Age-matched iron-deficient (ID) and control rats composed the other two groups. Fourteen days of repletion with 35 mg/kg Fe dietary treatment were adequate to normalize hematology, brain microsomal and cytosolic Fe and brain ferritin (Experiment 1). Brain transferrin concentrations in REPL rats, however, were significantly above the levels of controls. Regional brain iron decreased heterogeneously due to dietary iron deficiency (Experiment 2), with some regions having a propensity to keep iron (e.g., substantia nigra, pons, and thalamus) and others losing significant amounts of iron (cortex and hippocampus). Ferritin and Tf concentrations also varied significantly across brain regions in ID and control rats. The hippocampus had the most dramatic Tf response to iron deficiency with elevations of approximately 100%, whereas other regions, except striatum, were unaffected. The brain of developing rats thus distributes iron and iron regulatory proteins differently from the brain of adult rats and is quite avid in its reacquisition of iron during iron therapy.

Anemia, Iron-Deficiency↗

PubMed2002

The effects of iron deficiency and iron and zinc supplementation on rat hippocampus ferritin.

Iron deficiency (ID), the most prevalent nutritional disorder in the world, impairs cognition in early development. The involvement of hippocampus in cognition has prompted investigation into distribution of the iron storage protein ferritin (FER) in rat hippocampus. (a) In normal rats, FER positive cells appeared first in lateral CA3 and hilus of dentate gyrus and then spread over the entire mossy fiber (MF) system. No such spread was observed in CA1 field. (b) Nutritional iron deficiency retarded development of FER in the MF system. No change in FER was observed in CA1 field. (c) Zinc distribution can be altered by iron deficiency. Thus, the effect of zinc added to iron supplementation was tested in iron-deficient rats. Significant FER recovery was observed only in hippocampal MF of rats receiving both zinc and iron. It is apparent that for accelerating recovery of hippocampal function in iron deficiency, both zinc and iron are required.

Animals↗

PubMed2003

Non-anemic iron deficiency, oral iron supplementation, and oxidative damage in college-aged females.

Oxidative damage, as indicated by protein carbonyl and lipid hydroperoxide concentrations, was assessed in the plasma of college-aged females with adequate iron status and with non-anemic iron deficiency before and after eight weeks of iron supplementation. At baseline, the mean serum ferritin, iron, transferrin saturation, and total iron binding capacity of the iron deficient group (n = 13) was significantly different from the iron adequate controls (n = 24). Mean plasma lipid hydroperoxide and protein carbonyl concentrations did not differ between groups at baseline. Following eight weeks of iron supplementation, the mean serum ferritin, iron, and transferrin saturation significantly increased and the total iron binding capacity significantly decreased in the iron deficient group. No significant differences in plasma lipid hydroperoxide or protein carbonyl concentrations were found between groups at the end of the study period. When plasma lipid hydroperoxide and protein carbonyl concentrations of subjects within groups were compared at the start versus at the end of the study, no significant differences were found for either group. Neither non-anemic iron deficiency nor its treatment with oral iron supplements is associated with oxidative damage in the plasma of college-aged females.

Adult↗

PubMed1999

Erythropoietin hyporesponsiveness: from iron deficiency to iron overload.

Iron deficiency is the most frequently encountered cause of suboptimal response to recombinant human erythropoietin (rHuEPO). Carefully assessing iron status is of paramount importance in chronic renal failure patients prior to or during rHuEPO therapy. Because there is great need for iron in the EPO-stimulated erythroid progenitors, it is essential that serum ferritin and transferrin saturation levels should be maintained over 300 microg/liter and 30%, respectively. Investigators have shown that oral iron is unlikely to keep pace with the iron demand for an optimal rHuEPO response in uremics. Therefore, patients with iron deficiency will always require intravenous iron therapy. The early and prompt iron supplementation can lead to reductions in rHuEPO dose and hence cost. After the iron deficiency has been corrected or excluded, we must remember all of the possible causes of hyporesponsiveness in every rHuEPO-treated patient. As dose requirements vary, it is not clear which dose of rHuEPO causes this hyporesponsiveness. However, if the patient with iron repletion does not respond well after the induction period, the major causes blunting the response to rHuEPO should be investigated. Most factors are reversible and remediable, except resistant anemia associated with hemoglobinopathy or bone marrow fibrosis, which requires a further increase in the rHuEPO dose. By means of early detection and correction of the possible causes, the goal of increasing therapeutic efficacy can be achieved. Iron overload may lead to an enhanced risk for infection, cardiovascular complication, and cancer. Over-treatment with iron should be avoided in dialysis patients, despite the fact that the safe upper limit of serum ferritin to avoid iron overload is not clearly defined. On the other hand, functional iron deficiency may develop even when serum ferritin levels are increased. Controversy remains as to whether intravenous iron therapy can overcome this form of hyporesponsiveness in iron-overloaded patients. Moreover, a treatment option of iron supplementation is not warranted in these patients, as the potential hazards of iron overload will be worsened. We demonstrated that the mean hematocrit significantly increased from 25.1+/-0.9% to 31+/-1.2% after eight weeks of intravenous ascorbate therapy (300 mg three times a week) in 12 hemodialysis patients with serum ferritin levels of more than 500 microg/liter. The enhanced erythropoiesis paralleled with a rise in transferrin saturation (27.8+/-2.5% vs. 44.8+/-9.5%, P < 0.05) and reductions in erythrocyte zinc protoporphyrin (130+/-32 vs. 72+/-19 micromol/mol heme, P < 0.05) and monthly rHuEPO dose (24.2+/-4.5 vs. 16.8+/-3.4 x 10(3) units, P < 0.05) at the end of study. It is speculated that ascorbate supplementation not only facilitates the iron release from storage sites and its delivery to hematopoietic tissues, but also increases iron utilization in erythroid cells. Our study provides a more complete understanding of the pathogenesis of iron overload-related anemia and the development of an adjuvant therapy, intravenous ascorbic acid, to the existing treatments.

Aluminum↗

PubMed1991

[Iron stores, iron deficiency and iron supplementation].

In order to assess the prevalence of iron deficiency in the Danish population, a randomised cross sectional investigation was carried out one year after repealing of the order from 1939 concerning supplementing of corn products with iron. A randomised group of 198 persons divided into ten groups of 20 persons with equal numbers of men and women in the age group 20-69 years was submitted to determinations of serum-iron, serum-transferrin and serum-ferritin. The prevalence of iron deficiency as determined by serum-ferritin values of below 15 micrograms/l was 18% and 12% respectively, for women under and over 45 years while iron deficiency determined by transferrin saturation under 16% was 18% for both groups. 6% of the women under 45 years had severe iron deficiency as determined by low transferrin saturation and low ferritin. The prevalence among men was 1% and 3% as assessed by serum-ferritin levels and transferritin saturation. These results were compared with corresponding population investigations from Sweden where iron enrichment is the highest in the world and the sale of iron tablets is the greatest in the world. No significant differences in the frequency of latent iron deficiency could be demonstrated but the number of persons with severe iron depletion appears to be less in Sweden. Differences in the methodological procedures, however, cannot be excluded.

Adult↗

PubMed2001

Is There a Causal Relationship between Iron Deficiency or Iron-Deficiency Anemia and Weight at Birth, Length of Gestation and Perinatal Mortality?

An extensive literature review was conducted to identify whether iron deficiency, iron-deficiency anemia and anemia from any cause are causally related to low birth weight, preterm birth or perinatal mortality. Strong evidence exists for an association between maternal hemoglobin concentration and birth weight as well as between maternal hemoglobin concentration and preterm birth. It was not possible to determine how much of this association is attributable to iron-deficiency anemia in particular. Minimal values for both low birth weight and preterm birth occurred at maternal hemoglobin concentrations below the current cut-off value for anemia during pregnancy (110 g/L) in a number of studies, particularly those in which maternal hemoglobin values were not controlled for the duration of gestation. Supplementation of anemic or nonanemic pregnant women with iron, folic acid or both does not appear to increase either birth weight or the duration of gestation. However, these studies must be interpreted cautiously because most are subject to a bias toward false-negative findings. Thus, although there may be other reasons to offer women supplemental iron during pregnancy, the currently available evidence from studies with designs appropriate to establish a causal relationship is insufficient to support or reject this practice for the specific purposes of raising birth weight or lowering the rate of preterm birth.

Anemia↗

PubMed1994

New advances in iron metabolism, iron deficiency, and iron overload.

Rapid advances were made in understanding the molecular and cellular bases of iron metabolism and its disorders. Molecular mechanisms for the cellular uptake, storage, and utilization of iron were clarified in investigations of the structure and functions of transferrin, transferrin receptor, ferritin, erythroid delta-aminolevulinic acid synthase, and the RNA-binding protein termed the iron responsive-element binding protein. Evidence was obtained that a nuclear DNA-binding protein, NF-E2, may be involved in the regulation of both hemoglobin synthesis in erythroid cells and of iron absorption in the intestine. Clinically, progress was made in improving the diagnosis and management of both iron deficiency and iron overload, with studies of the usefulness of serum transferrin receptor measurements, of a new therapeutic preparation of iron using a "gastric delivery system," and of the development of new orally active iron-chelating agents.

Anemia, Iron-Deficiency↗