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PubMed1987

Macrophage function as studied by the clearance of 125I-labeled polyvinylpyrrolidone in iron-deficient and iron-replete mice.

This study evaluated the effects of iron deficiency and iron repletion on in vivo macrophage function determined by the clearance of 125I-labeled polyvinylpyrrolidone (PVP). Two experiments were done. There were four groups of C57BL/6 female mice in experiment 1: the iron-deficient (ID), pair-fed (PF), control (C) and the high iron (HI) groups. In experiment 2, there were three ID groups (severe to moderate anemia), three PF, one C and four ID groups that were fed adequate iron for 14 (R-14), 7 (R-7), 3 (R-3) days before or on the day of PVP injection (R-0). The overall rate of PVP clearance from blood was lower in ID than in C or PF groups. This clearance is expressed by a constant, K, calculated from natural log (ln) of the cpm and the time postadministration of PVP that blood was drawn. The theoretical individual macrophages function (alpha PVP), derived from K and the weights of body, spleen and liver, was also lower in ID than in C or PF groups. The impairment was most severe with the most severe iron deficiency. Repletion for 7 to 15 d before PVP administration resulted in a partial correction of the clearance. Moderate undernutrition in the PF group had no effect.

Animals↗
PubMed2004

The effect of Helicobacter pylori infection and dietary iron deficiency on host iron homeostasis: a study in mice.

BACKGROUND: Helicobacter pylori, which requires iron to survive, may cause host iron deficiency by directly competing with the host for available iron or by impairing iron uptake as a consequence of atrophy-associated gastric hypochlorhydria. The aim of this study was to examine the effect of H. pylori infection and dietary iron deficiency on host iron homeostasis in a mouse model. MATERIALS AND METHODS: H. pylori SS1-infected and uninfected C57BL/6 mice, fed either a normal diet or an iron-deficient diet, were assessed for iron status and infection-associated gastritis over a 30-week period. RESULTS: After 10 weeks, serum ferritin values were higher in H. pylori-infected mice than in uninfected controls, irrespective of dietary iron intake (p = .04). The infection-related increase in body iron stores persisted in the iron-replete mice but diminished over time in mice with restricted dietary iron intake (p < .0001). At 30 weeks serum ferritin levels were lower in these animals (p = .063). No significant difference in bacterial numbers was detected at the 30-week time point (p > .05) and the histological changes observed were consistently associated with infection (p < .01) and not with the iron status of the mice (p = .771). CONCLUSIONS: Infection with H. pylori did not cause iron deficiency in iron-replete mice. However, diminished iron stores in mice as a result of limited dietary iron intake were further lowered by concurrent infection, thus indicating that H. pylori competes successfully with the host for available iron.

Animals↗
PubMed1987

Iron deficiency anemia and iron therapy effects on infant developmental test performance.

The behavioral effects of iron deficiency and its treatment were evaluated in a double-blind randomized controlled community-based study of 191 Costa Rican infants, 12 to 23 months of age, with various degrees of iron deficiency. The Bayley Scales of Infant Development were administered before and both 1 week and 3 months after IM or oral administration of iron. Appropriate placebo-treated control infants were also tested. Infants with iron deficiency anemia showed significantly lower mental and motor test scores, even after considering factors relating to birth, nutrition, family background, parental IQ, and the home environment. After 1 week, neither IM nor oral iron treatments differed from placebo treatment in effects on scores. After 3 months, lower mental and motor test scores were no longer observed among iron-deficient anemic infants whose anemia and iron deficiency were both corrected (36%). However, significantly lower mental and motor test scores persisted among the majority of initially anemic infants (64%) who had more severe or chronic iron deficiency. Although no longer anemic, they still showed biochemical evidence of iron deficiency after 3 months of treatment. These persistent lower scores suggest either that iron therapy adequate for correcting anemia is insufficient to reverse behavioral and developmental disturbances in many infants or that certain ill effects are long-lasting, depending on the timing, severity, or chronicity of iron deficiency anemia in infancy.

Anemia, Hypochromic↗
PubMed2001

Iron deficiency and iron overload: effects of diet and genes.

Like most essential nutrients, Fe needs to be maintained in the body at a defined level for optimal health, with appropriate adaptation to varying Fe needs and supply. The primary mechanism for controlling Fe level is the regulation of Fe absorption. Several different proteins have been identified as contributors to the process. Despite a complex regulatory system, Fe disorders (both Fe deficiency and Fe overload) occur. Fe deficiency is a common problem worldwide, resulting from inadequate dietary Fe and blood loss. Complications include pre-term labour, developmental delay, and impaired work efficiency. No specific genetic syndromes causing isolated Fe deficiency have been described, but animal studies and clinical observations suggest that such a relationship may be a possibility. Conversely, the known causes of Fe overload are genetic. Fe overload is less common than Fe deficiency, but can result in serious medical complications, including cirrhosis, primary liver cancer, diabetes, cardiomyopathy and arthritis. The most common and best characterized syndrome of Fe overload is hereditary haemochromatosis (HHC), an autosomal recessive disorder. Mutations in the HFE protein cause HHC, but the clinical presentation is variable. Of particular interest is the factor that some FIFE genotypes appear to be associated with protection from Fe deficiency. Other genetic variants in the regulatory pathway may influence the likelihood of Fe deficiency and Fe overload. Studies of genetic variants in HFE and other regulatory proteins provide important tools for studying the biological processes in Fe regulation. This work is likely to lead to new insights into Fe disorders and potentially to new therapeutic approaches. It will not be complete, however, until coordinated study of both genetic and nutritional factors is undertaken.

Anemia, Iron-Deficiency↗
PubMed1982

Mitochondrial NADH dehydrogenase in iron-deficient and iron-repleted rat muscle: an EPR and work performance study.

Iron may affect both respiratory O2 transport and mitochondrial electron transport in the performance of muscle work. This study was designed to elucidate the molecular defect of iron-deficient work performance by identifying heretofore unmeasurable mitochondrial enzymes that are diminished by iron deficiency and may be restored by iron repletion. Female rats were made iron-deficient by dietary control and were repleted by oral iron. Iron deficiency reduced physical work capacity (treadmill running time), haemoglobin (Hb), and mitochondrial iron-sulphur (Fe-S) centres in heart and skeletal muscles; mitochondrial number was unaffected. Oral iron supplementation restored work capacity and Hb within 4 d to normal or near-normal levels, but in general Fe-S centres of mitochondria due to NADH dehydrogenase remained at iron-deficient levels. Subnormal concentrations of mitochondrial iron-dependent NADH dehydrogenase in muscle are not by themselves rate-limiting in work performance.

Anemia, Hypochromic↗
PubMed1979

Transferrin binding and iron transport in iron-deficient and iron-replete rat reticulocytes.

Three aspects of iron metabolism were studies in reticulocytes from iron-deficient, phlebotomized, and phenylhydrazine-treated rats: (1) the number of transferrin binding sites; (2) the uptake of 59Fe-transferrin; and (3) the ability of cytosol to mobilize 59Fe from 59Fe-labeled reticulocyte plasma membrane. The number of transferrin binding sites, assayed by measuring the binding of 125I-labeled transferrin to reticulocytes, were similar in iron-deficient and phlebotomy-induced reticulocytes, 66,000 and 75,000 binding sites/cell, respectively, but were about doubled, 120,000 binding sites/cell, in phenylhydrazine-induced reticulocytes. Uptake of 59Fe into iron-deficient reticulocytes was about one-half that for phlebotomy-induced reticulocytes and one-quarter that for phenylhydrazine-induced reticulocytes, the rates of uptake being measured as 21,540, 41,233, and 79,600 molecules of 59Fe per minute per cell, respectively. The mobilizing activity of cytosol free iron-deficient reticulocytes was also about one-half that of cytosol from phlebotomy-induced reticulocytes and about one-quarter that of cytosol from phenylhydrazine-induced reticulocytes. These results indicate that instead of a compensatory increase in these aspects of iron metabolism, the iron-deficient reticulocyte had a decreased ability to transport iron.

Anemia, Hypochromic↗
PubMed1994

The effects of iron deficiency and iron overload on cell-mediated immunity in the mouse.

The influence of Fe status on cell-mediated immunity was studied in weanling mice fed on Fe-deficient (7 mg Fe/kg), Fe-sufficient (120 mg Fe/kg) and high-Fe (3000 or 5000 mg Fe/kg) diets for 7 weeks. The contact sensitivity (CS) response to dinitrofluorobenzene (DNFB), the in vivo delayed-type hypersensitivity (DTH) response to sheep erythrocytes (SRBC) and the ability of primed spleen cells to transfer DTH response to naive normal mice were suppressed in mice consuming the Fe-deficient diet. High-Fe diets (3000 or 5000 mg Fe/kg) selectively suppressed the CS response to DNFB, but the DTH response to SRBC or the transfer of DTH response by primed spleen cells to naive normal mice remained normal. Spleen cell functions associated with the expression of class II major histocompatibility (MHC) surface antigens, concanavalin A-induced interleukin-2 (IL-2) secretion or the antigen-presenting cell (APC) ability to stimulate antigen-dependent proliferation of an SRBC-specific helper T-lymphocyte clone were not altered by Fe status. However, consistent with the suppressed DTH response in the Fe-deficient mice was the suppressed concanavalin A-induced T-lymphocyte blastogenesis and the interferon-gamma (INF-gamma) production by spleen cells from mice fed on the Fe-deficient diet. Spleen cells from mice fed on excess levels of Fe in the diet secreted less INF-gamma than the control mice, although T-lymphocyte proliferation remained unaffected. Suppression of the cellular immune response associated with Fe deficiency may be related in part to impaired T-lymphocyte proliferation and INF-gamma secretion rather than to deficits in IL-2 secretion or APC function.

Animals↗
PubMedDate not supplied

Effects of iron deficiency and iron overload on manganese uptake and deposition in the brain and other organs of the rat.

Manganese (Mn) is an essential trace element at low concentrations, but at higher concentrations is neurotoxic. It has several chemical and biochemical properties similar to iron (Fe), and there is evidence of metabolic interaction between the two metals, particularly at the level of absorption from the intestine. The aim of this investigation was to determine whether Mn and Fe interact during the processes involved in uptake from the plasma by the brain and other organs of the rat. Dams were fed control (70 mg Fe/kg), Fe-deficient (5-10 mg Fe/kg), or Fe-loaded (20 g carbonyl Fe/kg) diets, with or without Mn-loaded drinking water (2 g Mn/L), from day 18-19 of pregnancy, and, after weaning the young rats, were continued on the same dietary regimens. Measurements of brain, liver, and kidney Mn and nonheme Fe levels, and the uptake of 54Mn and 59Fe from the plasma by these organs and the femurs, were made when the rats were aged 15 and 63 d. Organ nonheme Fe levels were much higher than Mn levels, and in the liver and kidney increased much more with Fe loading than did Mn levels with Mn loading. However, in the brain the increases were greater for Mn. Both Fe depletion and loading led to increased brain Mn concentrations in the 15-d/rats, while Fe loading also had this effect at 63 d. Mn loading did not have significant effects on the nonheme Fe concentrations. 54Mn, injected as MnCl2 mixed with serum, was cleared more rapidly from the circulation than was 59Fe, injected in the form of diferric transferrin. In the 15-d-rats, the uptake of 54Mn by brain, liver, kidneys, and femurs was increased by Fe loading, but this was not seen in the 63-d rats. Mn supplementation led to increased 59Fe uptake by the brain, liver, and kidneys of the rats fed the control and Fe-deficient diets, but not in the Fe-loaded rats. It is concluded that Mn and Fe interact during transfer from the plasma to the brain and other organs and that this interaction is synergistic rather than competitive in nature. Hence, excessive intake of Fe plus Mn may accentuate the risk of tissue damage caused by one metal alone, particularly in the brain.

Administration, Oral↗
PubMed1998

Intracardiac iron distribution in newborn guinea pigs following isolated and combined fetal hypoxemia and fetal iron deficiency.

Myocardial iron deficiency complicates chronic intrauterine hypoxemia during diabetic pregnancies. To understand the effect of both conditions during fetal life on intracardiac iron prioritization, we measured heart myoglobin, cytochrome c, and elemental iron concentrations in six iron-deficient, hypoxic, five iron-sufficient, hypoxic, six iron-deficient, normoxic, and six iron-sufficient, normoxic newborn guinea pigs. The iron-deficient, hypoxic group had lower heart iron (p = 0.03) but higher myoglobin concentration (p < 0.0001) when compared with the iron-sufficient, normoxic group. The percentage of iron incorporated into myoglobin was higher than control in the iron-deficient, hypoxic group (23.2+/-7.2% vs. 5.2+/-0.8%; p < 0.001) and increased as total heart iron decreased (r = 0.97; p < 0.001). In contrast, heart cytochrome c concentration was lower than control in the iron-deficient, hypoxic group (p = 0.01), with equal percentages of heart iron incorporated into cytochrome c. This intracellular prioritization of myocardial iron to myoglobin and away from cytochrome c following combined fetal hypoxemia and iron deficiency may represent an adaptive mechanism to preserve myocardial tissue oxygenation, although at the expense of oxidative phosphorylative capability.

Animals↗
PubMed1975

Utilization of dietary calcium by iron-deficient rats.

Iron deficiency causes cytological and enzymic changes in the gastrointestinal mucosa of animals and man that can be expected to impair the digestion and absorption of other nutrients. In experiment 1, healthy, weanling, female rats were grouped into pair-mates and pair-fed either an iron-deficient or an iron-supplemented diet for 19 weeks. In experiment 2, iron-deficient offspring reared by iron-deficient females were grouped into pair-mates and pair-fed either an iron-deficient or an iron-supplemented diet for 15 weeks. In experiment 1, apparent absorption of calcium was significantly depressed in week 9 (p less than 0.001) and slightly depressed in weeks 10 and 11. In experiment 2, the apparent absorption of calcium was significantly (p less than 0.001) depressed in weeks 6, 13, and 14. Absorption was not measured in other weeks in these experiments. The concentrations of calcium and magnesium were consistently higher in the fecal dry matter of the iron deficient rats in both experiments. It was concluded that any defects in digestion and absorption by the iron-deficient rats was confined primarily to the mineral nutrients because in both experiments apparent absorption of dry matter was consistently higher in these animals compared to their iron-supplemented pair-mates.

Animals↗
PubMed2004

[Clinical experiences of the medication to taste disturbance by serum trace deficiency, especially serum iron deficiency].

Serum zinc deficiency is known to be a major cause of taste disturbances, but the effects of serum iron deficiency on taste disturbances are not widely known. In the present study, we clinically investigated the relationship between taste disturbances and serum iron deficiency as well as the results of pharmacological therapy. The clinical and serological test results of 25 patients with serum iron deficiency (3 men and 22 women; mean age +/- SD, 56.1 +/- 16.5 years) were reviewed at the Department of Otolaryngology, Hospital of Hyogo College of Medicine. All of the patients had been seen at the hospital between January 1999 and February 2003. Electrogustometry (EGM) and the filter paper disc method (FPD) were used to measure taste function. The patients were treated with iron and zinc supplements. The age distribution of the patients peaked at the ages of 40 and 70 years. The ratio of males to females was 1:7. Based on the EGM results, 70% of the patients exhibited taste disturbances. The FPD results showed that the recognition threshold of sour tastes was slightly higher than that of the other tastes. No significant difference in the results of treatment was seen, regardless of the duration of the deficiency. These results suggest that treatment with iron and zinc medicine is useful for correcting taste disturbances caused by serum deficiencies of trace elements.

Adult↗
PubMed2000

Both iron deficiency and daily iron supplements increase lipid peroxidation in rats.

Numerous studies have shown that iron-loaded diets increase markers of lipid peroxidation in rats, but few have addressed the effects of oral iron supplements on these markers. We investigated the effects of daily and intermittent iron supplements on iron and vitamin E status, and lipid peroxidation. Iron supplements were administered in doses equivalent to those often given to pregnant women in the developing world. In Study 1, iron-deficient (D) and iron-normal (N) rats were fed either 0 or 8000 microgram of supplemental iron daily for 21 d. In Study 2, D rats were fed either the same supplements daily or once every 3 d (8 supplements total). Lipid peroxidation was assessed by breath ethane and pentane and by malondialdehyde (MDA) (using GC-MS). In Study 1, daily supplemented N and D rats had liver nonheme iron concentrations that were 1.8- and 2.7-fold higher, respectively, than those in unsupplemented N rats. Breath ethane levels were also higher in supplemented rats (P < 0.05), but MDA (in plasma, liver, kidney) and liver vitamin E did not differ. Unexpectedly, severely D, anemic rats had significant elevations in the levels of breath ethane, liver MDA and kidney MDA. In Study 2, liver iron and breath ethane decreased progressively (P < 0.05) from 1 d to 3 d after the last iron dose in intermittently supplemented rats. We conclude that iron deficiency results in lipid peroxidation, but that its correction with daily iron supplements results in abnormal iron accumulation and increased lipid peroxidation in rats. These effects are mitigated by intermittent iron supplementation.

Animals↗
PubMed2000

Structural and cellular adaptation of duodenal iron uptake in rats maintained on an iron-deficient diet.

Iron deficiency induced in rats maintained on a commercial diet with a low iron content has been used to investigate adaptive mechanisms that enhance duodenal iron uptake. These adaptive changes have been divided into those that result from changes in villus surface area (structural adaptation) and those that reflect changes in the way individual enterocytes express iron transport function (cellular adaptation). Cellular adaptation was assessed by carrying out microdensitometry of autoradiographs prepared from duodenal tissue previously incubated for 5 min in 200 micromol/l 59Fe2+-ascorbate. Structural adaptation was studied by performing image analysis of microdissected and sectioned villi. Cellular adaptation involved increased iron uptake by enterocytes present in the lower villus. Thus iron deficiency resulted in a threefold enhanced expression of uptake in the lower 100 microm villus (3.9+/-2.4 versus 12.6+/-1.5 arbitrary units, P<0.001). Maximal uptake was reached in the upper region of both control and iron-deficient villi, but iron deficiency had no effect on cellular uptake at this part of the villus. Structural adaptation involved the lengthening (+16%, P<0.05) and broadening (+14%) of villi in the duodenum of iron-deficient rats. The resultant expansion in villus area caused a further increase in uptake that was mostly expressed in the upper villus. Maximal uptake corrected for structure occurred in the middle third of villi from control and iron-deficient rats. Cellular plus structural adaptation produced a twofold increase in iron uptake. More than half of this effect was caused by changes in villus structure. [3H]Thymidine labelling experiments revealed a slightly earlier expression of enterocyte iron uptake in iron deficiency.

Adaptation, Physiological↗