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PubMed1983

Reduced plasma lecithin cholesterol acyl transferase activity in rats fed iron-deficient diets.

An iron-deficient diet containing no fat (FF-Fe) or containing either 14% hydrogenated coconut oil (HCNO-Fe) or 14% corn oil (CO-Fe) was fed to separate groups of rats for 10 weeks. In the control group, the corresponding iron-supplemented diets were fed FF+Fe, HCNO+Fe, CO+Fe. When rats were fed iron-deficient diets, their plasma lecithin cholesterol acyl transferase (LCAT) activity was significantly reduced as compared to controls. Their plasma also contained releatively more cholesteryl esters (CE) than free cholesterol (CH). In rats fed FF+Fe and CO+Fe diets, plasma contained similar levels of CE and CH. In those fed HCNO+Fe diet, plasma had 40% less Ce than CH. Red cell CH content was significantly greater in the CO-Fe group. Iron deficiency, as indicated by low blood hemoglobin (Hb) and hematocrit (Hct) values, was also observed only in this group. The triglyceride and phospholipid contents of plasma in rats fed iron-deficient diets were significantly lower than of those in the control groups. Thus, changes in LCAT activity and CE/CH ratio in plasma showed the effect of iron-deficient diet consumption even before the blood Hb and Hct levels were reduced.

Animals↗
PubMed1998

Transferrin response in normal and iron-deficient mice heterozygotic for hypotransferrinemia; effects on iron and manganese accumulation.

Hypotransferrinemia is a genetic defect in mice resulting < 1% of normal plasma transferrin (Tf) concentrations; heterozygotes for this mutation (+/hpx) have low circulating Tf concentrations. These mice provide a unique opportunity to examine the developmental pattern and response of Tf to iron-deficient diets, and furthermore, to address the controversial role of Tf in Mn transport. Twenty-three weanling +/hpx mice and forty-five wild-type BALB/cJ mice were either killed at weaning or fed diets containing either 13 or 72 mg kg-1 Fe, and killed after four or eight weeks. Plasma Tf concentrations were lower in +/hpx mice, plasma Tf nearly doubled and liver Tf was only 50% of normal in response to iron deficiency. Brain iron concentration did not correlate significantly with either plasma Tf or TIBC. However, iron accumulation into brain continued with iron deficiency whereas most other organs had less iron. These results imply that either there is a selected targeting of iron to the brain by plasma Tf or there is an alternative iron delivery system to the brain. Furthermore, we observed no differences in tissue distribution of 54Mn despite the differences in circulating Tf concentrations and body iron stores; this suggests that there are non-Tf dependent mechanisms for Mn transport.

Animals↗
PubMed1998

Influence of nutritional iron deficiency development on some aspects of iron, copper and zinc metabolism.

This paper examines the development of iron (Fe) deficiency and its possible interactions with trace elements such as zinc (Zn) and copper (Cu) by investigating iron-deficient and control rats. The effects of iron deficiency were studied at day 0, 10, 20, 30 and 40 in rats fed on an iron-free diet (diet ID). It was found that the critical period in the development of nutritional iron deficiency occurs after 30 to 40 days without iron supplementation. At this time the organism is unable to maintain haemoglobin levels without endangering the iron-dependent enzymatic groups which are essential for life. It was also demonstrated that in a situation of iron deficiency, there occurs a greater absorption of copper, while that of zinc remains unchanged. As iron deficiency progresses, the levels of copper in the spleen and the sternum increase. It is apparent that iron deficiency provokes more marked alterations in the metabolism of copper than of zinc.

Animal Nutritional Physiological Phenomena↗
PubMed1996

[Changes in brain monoamine neurotransmitter in iron deficiency nonanemic rats].

An iron deficiency nonanemic rat model was established by feeding with low-iron diet (11.9 mg/kg) to study if there exists biochemical abnormality in brain tissues. Iron contents of the brain, activities of monoamine oxidase (MAO) in the corpus striatum, and the contents of monoamine neurotransmitter and its metabolite in the cerebral cortex and hippocampus were determined by DCP-AES technique, enzyme histochemical method, and high performance liquid chromatography with electrochemical detection (HPLC-ECD), respectively. Results showed that iron contents and activities of MAO in brain tissues of iron deficiency nonanemic rats reduced significantly, and contents of norepinephrine (NE) and 5-hydroxytryptamine (5-HT) in cerebral cortex were significantly higher than those of controls, while 5-hydroxydroxytryptamine acid (5-HIAA) metabolite of 5-HT in the hippocampus was lower than that of controls. It indicated that there existed metabolic abnormality of monoamine neurotransmitter in the brain tissues of iron deficiency nonanemic rats. Also, this study laid a biochemical basis for abnormal mental and behavioral development caused by iron deficiency.

Animals↗
PubMed2002

Low income postpartum women are at risk of iron deficiency.

We estimated the prevalence of postpartum iron deficiency, anemia and iron deficiency anemia in the United States and compared risk of iron deficiency between women 0-24 mo postpartum (n = 680) and never-pregnant women, 20-40 y old (n = 587). We used data from National Health and Nutrition Examination Survey, 1988-1994. Iron deficiency was defined as abnormal values for > or = 2 of 3 iron status measures (serum ferritin, free erythrocyte protoporphyrin, transferrin saturation). Iron deficiency prevalences for women 0-6, 7-12 and 13-24 mo postpartum were 12.7, 12.4 and 7.8%, respectively, and 6.5% among never-pregnant women. After adjustment for confounding, the risk of iron deficiency among women with a poverty index ratio < or = 130% who were 0-6, 7-12 and 13-24 mo postpartum was 4.1 (95% confidence interval 2.0, 7.2), 3.1 (1.3, 6.5) and 2.0 (0.8, 4.1) times as great, respectively, as never-pregnant women with a poverty index ratio > 130%, but risk was not elevated for never-pregnant women with a poverty index ratio < or = 130%. Compared with the same referent, the risk of iron deficiency was not meaningfully different for women with a poverty index ratio > 130% who were 0-6, 7-12 or 13-24 mo postpartum. Given that low income postpartum women bear a substantially greater iron deficiency risk than never-pregnant women, more attention should be given to preventing iron deficiency among low income women during and after pregnancy.

Anemia, Iron-Deficiency↗
PubMed2005

N-terminal processing of Lhca3 Is a key step in remodeling of the photosystem I-light-harvesting complex under iron deficiency in Chlamydomonas reinhardtii.

Iron deficiency induces a remodeling of the photosynthetic apparatus in Chlamydomonas reinhardtii. In this study we showed that a key mechanistic event in the remodeling process of photosystem I (PSI) and its associated light-harvesting proteins (LHCI) is the N-terminal processing of Lhca3. N-terminal processing of Lhca3 is documented independently by two-dimensional gel electrophoresis and tandem mass spectrometric (MS/MS) analysis as well as by quantitative comparative MS/MS peptide profiling using isotopic labeling of proteins. Dynamic remodeling of the LHCI complex under iron deficiency is further exemplified by depletion of Lhca5 and up-regulation of Lhca4 and Lhca9 polypeptides in respect to photosystem I. Most importantly, the induction of N-terminal processing of Lhca3 by progression of iron deficiency correlates with the functional drop in excitation energy transfer efficiency between LHCI and PSI as assessed by low temperature fluorescence emission spectroscopy. Using an RNA interference (RNAi) strategy, we showed that the truncated form of Lhca3 is essential for the structural stability of LHCI. Depletion of Lhca3 by RNAi strongly impacted the efficiency of excitation energy transfer between PSI and LHCI, as is the case for iron deficiency. However, in contrast to iron deficiency, comparative MS/MS peptide profiling using isotopic labeling of proteins demonstrated that RNAi depletion of Lhca3 caused strong reduction of almost all Lhca proteins in isolated PSI particles.

Amino Acid Sequence↗
PubMed1980

Manifestation of iron deficiency at various levels of dietary iron intake.

The purpose of this study was to determine the interrelationships between iron stores, serum iron, hemoglobin, myoglobin, and cytochrome c under conditions of iron deficiency that did not interfere with normal growth. Rats were given diets containing from 7 to 500 mg iron per kilogram of diet during a period of 3 weeks of rapid growth between weaning at 21 days and approaching sexual maturity at 42 days. We found that the level of iron intake required for a maximum concentration of hemoglobin was similar to that which results in a maximum level of tissue cytochrome c. The severity of iron deficiency anemia was proportionally similar to the degree of depletion of muscle cytochrome c at all levels of iron intake below 25 mg/kg diet. The results indicate that even the mildest degree of nutritional iron deficiency anemia also affected tissue cytochrome c and could impair cytochrome-dependent mitochondrial function.

Anemia, Hypochromic↗
PubMed1993

Cause and cure for iron deficiency in toddlers.

Iron deficiency is the commonest cause of anaemia in Britain. Maureen B Duggan asks: How does toddler iron deficiency aris? How is it reliably diagnosed? And how can it be prevented in the community? Is iron supplementation of foods, especially of breast milk substitutes and follow-on formulae important in communities at risk?

Anemia, Hypochromic↗
PubMed2003

Iron deficiency: global prevalence and consequences.

Iron deficiency is considered to be one of most prevalent forms of malnutrition, yet there has been a lack of consensus about the nature and magnitude of the health consequences of iron deficiency in populations. This paper presents new estimates of the public health importance of iron-deficiency anemia (IDA), which were made as part of the Global Burden of Disease (GBD) 2000 project. Iron deficiency is considered to contribute to death and disability as a risk factor for maternal and perinatal mortality, and also through its direct contributions to cognitive impairment, decreased work productivity, and death from severe anemia. Based on meta-analysis of observational studies, mortality risk estimates for maternal and perinatal mortality are calculated as the decreased risk in mortality for each 1 g/dl increase in mean pregnancy hemoglobin concentration. On average, globally, 50% of the anemia is assumed to be attributable to iron deficiency. Globally, iron deficiency ranks number 9 among 26 risk factors included in the GBD 2000, and accounts for 841,000 deaths and 35,057,000 disability-adjusted life years lost. Africa and parts of Asia bear 71% of the global mortality burden and 65% of the disability-adjusted life years lost, whereas North America bears 1.4% of the global burden. There is an urgent need to develop effective and sustainable interventions to control iron-deficiency anemia. This will likely not be achieved without substantial involvement of the private sector.

Adolescent↗
PubMed1987

Iron deficiency in adolescent endurance athletes.

Iron deficiency with or without anemia may impair athletic performance. Although previous reports suggest a high incidence of iron deficiency in adolescent athletes, the recommendations for routine screening are unclear. In this study, high school male and female cross-country runners were evaluated by determining serum ferritin, hemoglobin, and red blood cell indexes during an 11-week competitive season. At the beginning of the season one of 30 males and eight of 20 females had iron deficiency, defined as a ferritin level greater than or equal to 12 ng/ml. By the end of the season four additional males and another female became iron deficient, for an overall incidence of 17% in males and 45% in females. Of the 26 runners who were evaluated throughout the season, ferritin levels fell in all nine females and in 14 of 17 males. Iron-deficiency anemia was not observed in any subject. These findings suggest that nonanemic iron deficiency is common in adolescent runners. Although iron deficiency is more common in females, one of every five males was iron depleted by the close of the season. Preseason screening alone is shown to be inadequate for detecting iron-deficient athletes as five runners with low ferritin levels were not identified on the initial evaluation.

Adolescent↗
PubMed1992

[Prevalence and pathogenesis of iron deficiency in Japanese women (1981-1991)].

Iron deficiency anemia is the most prevalent among form of anemia in the world. In Japan, there is no overall report concerning prevalence and pathogenesis of iron deficiency. We estimated the prevalence of iron deficiency from the results of a survey of 3,015 Japanese women. The reference range for hemoglobin was derived from the average value of subjects with normal iron status (> or = 16% of transferrin saturation and > or = 12 ng/ml of serum ferritin). Using these reference standards, the prevalence of iron deficiency anemia, latent iron deficiency, storage iron deficiency, normal and others were 8.5%, 8.0%, 33.4%, 43.6% and 6.5%, respectively. The prevalence of iron deficiency anemia increased beginning in early lower teen girls, was highest in high teen-girls and, young women and decreased in elderly women. In elderly women, the cause of iron deficiency was often obvious associated with anemia of chronic disorders. The strategy for iron deficiency was discussed concerning iron fortification, mega-ingestion of vitamin C and low dose administration of iron tablets in the higher incidence group.

Adolescent↗
PubMedDate not supplied

Interleukin 2 production in iron-deficient children.

The relationship between iron status and capacity for IL-2 production by lymphocytes was assessed in 81 children from 6 mo to 3 yr of age selected at random from a population with low socioeconomic status, undergoing free systematic examination in four children's health centers in the Paris area. Iron deficiency was defined by the existence of at least two abnormal values among the three indicators of iron status: serum ferritin level less than or equal to 12 micrograms/L, transferrin saturation less than 12%, and erythrocyte protoporphyrin concentration greater than 3 micrograms/g hemoglobin. According to this definition, 53 children were classified as iron deficient and 28 as iron sufficient. No differences were observed between the iron-deficient and iron-sufficient groups in terms of the IL-2 concentration without stimulation by PHA. IL-2 production by lymphocytes stimulated with PHA, as well as the stimulation index (ratio of IL-2 concentration following stimulation by PHA to that of IL-2 concentration without stimulation by PHA) were significantly lower in iron-deficient children. The reduction in IL-2 production by activated lymphocytes observed in our study of iron-deficient children may be responsible for impairments in immunity found by other authors, particularly in cell-mediated immunity.

Anemia, Hypochromic↗
PubMed1972

Activity pattern of iron-deficient rats.

Iron-deficient rats appear to have a decrease in total activity and a disorder of diurnal rhythm. These are reversed by the administration of iron. The results may be relevant to the symptomatology of patients with iron deficiency anaemia.

Anemia, Hypochromic↗
PubMed1990

Iron deficiency: improved exercise performance within 15 hours of iron treatment in rats.

We tested the hypothesis that a very rapid improvement in exercise performance of iron-deficient rats after treatment with iron might reveal a rate-limiting role of ionic iron as an enzyme cofactor in energy metabolism. Rats were given iron-deficient or control diets after weaning at 21 d of age and intraperitoneal iron dextran (50 mg/kg) at 45 d of age. Time to fatigue during an easy walking exercise (endurance) was measured 15 and 18 h after iron dextran or saline injection. Endurance increased more than threefold compared to the saline-treated, iron-deficient animals without a significant change in hemoglobin concentration. This prompt improvement suggests that lack of cofactor iron might play a metabolically important role in impairing exercise performance in the severely iron-deficient rat.

Alcohol Oxidoreductases↗
PubMed1992

Hematologic features of iron deficiency anemia in llamas.

Iron deficiency anemia was identified and characterized in three 14 to 29-month-old male llamas (llama Nos. 1-3) from separate herds in Colorado. The identification of iron deficiency anemia was based on hypoferremia (serum iron = 20-60 micrograms/dl), erythrocytic features, and hematologic response to iron therapy. The anemia was moderate and nonregenerative and characterized by erythrocyte hypochromia, microcytosis (mean cell volume = 15-18 fl), and decreased mean corpuscular hemoglobin concentration (36.0-41.0 g/dl). Morphologic features unique to llamas with iron deficiency anemia included irregular distribution of hypochromia within erythrocytes and increased folded cells and dacryocytes. The cause of iron deficiency was not determined. The llamas were treated with various doses and schedules of parenteral iron dextran. Two of the llamas were monitored for up to 14 months after the start of iron therapy and experienced increases in hematocrit and mean cell volume values. In one llama, progressive replacement of microcytic cells with normal cells was visualized on sequential erythrocyte volume distribution histograms following iron therapy.

Anemia, Hypochromic↗