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PubMed1989

Transferrin receptor expression in normal, iron-deficient and iron-overloaded rats.

The distribution of transferrin receptor (TfR)-positive cells and their staining intensity were examined in the liver, duodenum, pancreas, spleen, kidney and brain of iron-deficient, iron-overloaded and normal Wistar rats to elucidate the regulatory effects of iron on TfR expression in vivo. Iron deficiency was produced by an iron-deficient food and water regimen, and iron overload by repeated intraperitoneal injections of ferric nitrilotriacetate (Fe3(+)- NTA) for 12 weeks. In iron-deficient rats, levels of hemoglobin (Hb = 5.9 +/- 0.7) and serum iron (SI = 29.9 +/- 4.4) were lower, and total iron-binding capacity (TIBC = 624.4 +/- 72.7) was higher than in normal rats (Hb = 15.6 +/- 0.9, SI = 206.5 +/- 20.5, TIBC = 416.0 +/- 56.0), and vice versa for SI (217.7 +/- 15.5) and TIBC (307.1 +/- 45.4) in iron-overloaded rats. In normal rats, TfR-positive granules were observed in hepatocytes and Kupffer cells of the liver, absorptive epithelium of the duodenum, acinar and Langerhans islet cells of the pancreas, macrophages and red pulp erythroblast of the spleen, and distal convoluted tubular epithelium of the kidney. Although the tissue distribution pattern of TfR-positive cells was similar in normal, iron-deficient and iron-overloaded rats, the staining intensity and number of TfR-positive cells were obviously higher in iron-deficient, and lower in iron-overloaded rats. We conclude that TfR expression is negatively regulated by the tissue concentration of iron.

Animals↗
PubMed1986

Iron deficiency and pseudo-iron deficiency in hospitalized horses.

Values for serum ferritin, serum iron, and serum total-iron binding capacity were determined in 100 hospitalized horses. Six foals had iron deficiency, as indicated by low serum ferritin and iron concentrations. Twenty-eight horses had low serum iron content and normal or high serum ferritin content and were considered to have pseudo-iron deficiency, possibly in response to infection. Ten horses had serum ferritin concentrations that were quite high, probably indicating iron overload.

Age Factors↗
PubMed2003

Iron status in Danish women, 1984-1994: a cohort comparison of changes in iron stores and the prevalence of iron deficiency and iron overload.

BACKGROUND AND OBJECTIVES: From 1954 to 1986, flour in Denmark was fortified with 30 mg carbonyl iron per kilogram. This mandatory enrichment of cereal products was abolished in 1987. The aim was to evaluate iron status in the Danish female population before and after abolishment of iron fortification. METHODS: Iron status, serum ferritin and haemoglobin, was assessed in population surveys in 1983-1984 comprising 1221 Caucasian women (1089 non-blood-donors, 130 donors) and in 1993-1994 comprising 1261 women (1155 non-blood-donors, 104 donors) equally distributed in age cohorts of 40, 50, 60 and 70 yr. RESULTS: In the 1984 survey, median ferritin values in the four age cohorts in non-blood-donors were 44, 57, 84 and 80 microg/L, and in the 1994 survey 40, 67, 97 and 95 microg/L, respectively. In 1984, premenopausal women had median ferritin of 43 microg/L and in 1994 of 39 microg/L (NS). In 1984, postmenopausal women had median ferritin of 75 microg/L and in 1994 of 93 microg/L (P < 0.0001). The prevalence of depleted iron stores (ferritin < 16 microg/L) was not significantly different in 1984 and 1994 either in premenopausal or in postmenopausal women. The prevalence of small + depleted iron stores (ferritin 300 microg/L) was unchanged in premenopausal women and had increased from 2.4% to 5.5% in postmenopausal women (P = 0.003). During the study period there was an increase in body mass index both in premenopausal and postmenopausal women (P = 0.06 and P = 0.008). Postmenopausal women displayed an increase in alcohol consumption (P < 0.0001) and a decrease in tobacco smoking (P < 0.001). In premenopausal women, there was a marked increase in the use of non-steroid anti-inflammatory drugs (P < 0.0001) in the study period, while this was unchanged in postmenopausal women. In premenopausal blood donors, median ferritin decreased from 1984 to 1994 (36 microg/L vs. 24 microg/L, P < 0.06). In postmenopausal blood donors, ferritin was not significantly different from 1984 to 1994 (50 microg/L vs. 41 microg/L, P = 0.15). CONCLUSION: Abolition of iron fortification reduced the median dietary iron intake in Danish women from 12 to 9 mg/d. Despite the absence of food iron fortification, from 1984 to 1994, body iron stores were unchanged in premenopausal women, whereas iron stores and the prevalence of iron overload in postmenopausal women had increased significantly. The reason appears to be the changes in dietary habits with a lower consumption of dairy products and eggs, which inhibit iron absorption, and a higher consumption of alcohol, meat and poultry, containing heme iron and enhancing iron absorption.

Adult↗
PubMed1998

Adaptive response of iron absorption to anemia, increased erythropoiesis, iron deficiency, and iron loading in beta2-microglobulin knockout mice.

Recently, a novel gene of the major histocompatibility complex (MHC) class I family, HFE (HLA-H), has been found to be mutated in a large proportion of hereditary hemochromatosis (HH) patients. Further support for a causative role of HFE in this disease comes from the observation that beta2-microglobulin knockout (beta2m-/-) mice, that fail to express MHC class I products, develop iron overload. We have now used this animal model of HH to examine the capacity to adapt iron absorption in response to altered iron metabolism in the absence of beta2m-dependent molecule(s). Mucosal uptake, mucosal transfer and retention of iron were measured in control and beta2m-/- mice with altered iron metabolism. Mucosal uptake of Fe(III), but not of Fe(II), by the mutant mice was significantly higher when compared with B6 control mice. Mucosal transfer in the beta2m-/- mice was higher, independent of the iron form tested. No significant differences were found in iron absorption between control and beta2m-/- mice when anemia was induced either by repetitive bleeding or by hemolysis through phenylhydrazine treatment. However, iron absorption in mice made anemic by dietary deprivation of iron was significantly higher in the mutant mice. Furthermore, the beta2m-/- mice manifested an impaired capacity to downmodulate iron absorption when dietary or parenterally iron-loaded. The expression of the defect in iron absorption in the beta2m-/- mice is quantitative, with iron absorption being excessively high for the size of body iron stores. The higher iron absorption capacity in the beta2m-/- mice may involve the initial step of ferric mucosal uptake and the subsequent step of mucosal transfer of iron to the plasma.

Adaptation, Physiological↗
PubMed1986

Effects of iron deficiency and chronic iron overloading on mitochondrial heme biosynthetic enzymes in rat liver.

The effects of iron deficiency and iron overloading on the mitochondrial enzymes involved in heme synthesis were studied in rat livers. The in vitro activities of several of the enzymes in this pathway were differentially influenced by the in vivo iron status of the animals. delta-Aminolevulinic acid synthase was slightly increased in iron-overloaded animals, but remained normal in iron-deficient animals (0.58 +/- 0.09, 0.91 +/- 0.19 and 0.61 +/- 0.12 nmol delta-aminolevulinic acid/mg per h). Copro- and protoporphyrinogen oxidase activities were increased (20 and 60% above controls) in iron-deficient animals. In contrast, coproporphyrinogen oxidase was decreased by 20%, while protoporphyrinogen oxidase remained unchanged in iron-overloaded rats. These variations of activities were not due to changes in the affinity of these enzymes toward their substrates, as coporphyrinogen had the same Km in each case (0.62 +/- 0.05 M) as did protoporphyrinogen (0.22 +/- 0.035 M). Thus, the Km did not vary with the treatment received by the animals. Ferrochelatase activity was measured by both the pyridine hemochromogen method and by measurement of zinc protoporphyrin with endogenous zinc as substrate. In all cases, ferrochelatase was found to be able to synthesize zinc protoporphyrin with endogenous zinc as substrate. However, the apparent Km of zinc chelatase for protoporphyrin was significantly different in the three groups of animals with Km,appProto, app = 2.4 +/- 0.1 10(-7), 4 +/- 0.3 10(-7) and 9.10 +/- 0.05 10(-7) M in iron-overloaded, control and iron-deficient animals, respectively. When ferrochelatase activity was measured by pyridine hemochromogen, identical results were observed in iron-deficient and control animals but decreased by 45% in iron-overloaded animals. The mitochondrial heme content was also decreased by 40% in iron-overloaded rats but unchanged in either iron-deficient or control rats.

5-Aminolevulinate Synthetase↗
PubMed2005

Iron status of the Taiwanese elderly: the prevalence of iron deficiency and elevated iron stores.

Iron status, prevalence of iron deficiency and elevated iron stores, and the effect of gastrointestinal ulceration on iron status in free-living Taiwanese elderly persons were all assessed in a nationally representative, cross-sectional nutrition survey--the Elderly NAHSIT. The survey included blood measurements of iron indices. Data were collected from 1202 elderly men and 1152 elderly women aged 65 years and older. Multiple iron measures, including serum ferritin (SF), transferrin saturation (Tsat), and hemoglobin were used to evaluate the prevalence of iron deficient erythropoiesis (ID) and iron deficiency anemia (IDA). Despite no routine practice of iron fortification in Taiwan, elderly subjects had a low prevalence of ID and IDA. The prevalence of ID was 2.3% in men and 1.4% in women. The prevalence of IDA was 2.5% in men and 2.0% in women. In contrast, 15.7% of men and 9.8% of women had elevated iron stores as diagnosed by SF>300 microg/L. Subjects with a history of gastrointestinal ulceration had significantly lower serum ferritin than those without ulcers, but the prevalence of anemia, ID and IDA was unaffected. In conclusion, elderly people in Taiwan are an iron-replete population with a high prevalence of elevated iron stores and a low prevalence of iron deficiency.

Aged↗
PubMed1989

Evidence for thyroid hormone deficiency in iron-deficient anemic rats.

Iron-deficient anemic rats have previously been shown to have low plasma levels of thyroid hormone and a poor plasma thyroid hormone response to acute cold exposure. As an initial exploration, we examined thyroid hormone metabolism during iron deficiency in age-matched rats from three aspects: 1) plasma TSH (thyrotropin, thyroid stimulating hormone), T4 (thyroxine) and T3 (triiodothyronine) responses to graded doses of exogenous TRH (thyrotropin releasing hormone), 2) plasma T3 kinetics, and 3) rates of hepatic T3 production. Iron-deficient anemic rats had lower basal TSH values and blunted TSH responses to intravenous TRH injection at three different doses (10, 25 and 50 ng TRH/100 g body wt). Iron-deficient anemic rats also had a significant decrease in plasma T3 turnover (42 vs. 88 ng/h in controls), and significantly lower hepatic T4-5'-deiodinase activities than controls [26 vs. 44.0 ng T3/(mg protein.20 min)]. Thus, decreased rates of T3 production in iron-deficient anemic rats, as documented by turnover studies, may be related to decreased deiodinase activity and reduced peripheral formation of T3. The dampened TSH responses to TRH further facilitate or perpetuate this T3 deficiency. We propose that this abnormal thyroid state is partially responsible for impaired thermogenesis in iron-deficiency anemia.

Anemia, Hypochromic↗
PubMed2003

Microarray analysis of the genome-wide response to iron deficiency and iron reconstitution in the cyanobacterium Synechocystis sp. PCC 6803.

A full-genome microarray of the (oxy)photosynthetic cyanobacterium Synechocystis sp. PCC 6803 was used to identify genes that were transcriptionally regulated by growth in iron (Fe)-deficient versus Fe-sufficient media. Transcript accumulation for 3,165 genes in the genome was analyzed using an analysis of variance model that accounted for slide and replicate (random) effects and dye (a fixed) effect in testing for differences in the four time periods. We determined that 85 genes showed statistically significant changes in the level of transcription (P </= 0.05/3,165 = 0.0000158) across the four time points examined, whereas 781 genes were characterized as interesting (P </= 0.05 but greater than 0.0000158; 731 of these had a fold change >1.25 x). The genes identified included those known previously to be Fe regulated, such as isiA that encodes a novel chlorophyll-binding protein responsible for the pigment characteristics of low-Fe (LoFe) cells. ATP synthetase and phycobilisome genes were down-regulated in LoFe, and there were interesting changes in the transcription of genes involved in chlorophyll biosynthesis, in photosystem I and II assembly, and in energy metabolism. Hierarchical clustering demonstrated that photosynthesis genes, as a class, were repressed in LoFe and induced upon the re-addition of Fe. Specific regulatory genes were transcriptionally active in LoFe, including two genes that show homology to plant phytochromes (cph1 and cph2). These observations established the existence of a complex network of regulatory interactions and coordination in response to Fe availability.

Cyanobacteria↗
PubMed2003

Different behaviour of 63Ni and 59Fe during absorption in iron-deficient and iron-adequate jejunal rat segments ex vivo.

Nickel exhibits low oral toxicity. It shares the absorptive pathways for iron, though there are substantial quantitative differences in handling of both metals. To analyse these differences more closely, jejunal segments from iron-deficient and iron-adequate rats were luminally perfused ex vivo with 59Fe and 63Ni at six different concentrations (1-500 micromo1/l) under steady state conditions. 59Fe over-all absorption increased 2.0-4.6-fold in iron-deficiency at luminal concentrations between 1 and 100 micromol/l, while 63Ni absorption increased to a much lower extent (2.6-fold at 1 micromol/l and 1.5-fold at higher luminal concentrations). Moreover, there was a 5-7-fold higher concentration for 63Ni in the jejunal tissue than in the absorbate at luminal concentrations above 50 micromol/l which was not observed at 1 micromol 63Ni/l and not for 59Fe. 63Ni tissue load showed a linear and a saturable fraction. In iron-deficiency the saturable 63Ni fraction increased 4-fold as compared to only 1.5-fold increments for 59Fe. Moreover, a substantially higher share of 63Ni was retained in the jejunal tissue at high as compare to low luminal concentrations after perfusion had been continued without luminal radioactivity. This was not found for 59Fe and suggests a concentration-dependent block of 63Ni export across the enterocytes' basolateral membrane. To explain these results one may speculate that 63Ni may bind more tightly to tissue ligands than 59Fe due to the higher thermodynamic and kinetic stability of nickel complexes. In particular, nickel may bind to a basolateral population of metal carriers and block its own basolateral transfer in a concentration-dependent manner. Tight 63Ni binding to non-specific jejunal ligands is responsible for the unaltered high linear fraction of jejunal 63Ni load in iron-deficient and iron-adequate segments. Binding of 63Ni to food and tissue ligands in the small intestine may, thus, be a likely explanation for the low oral nickel toxicity.

Animals↗
PubMedDate not supplied

The IgM and IgG antibody responses in iron-deficient and iron-loaded mice.

The humoral immune response was evaluated in male CD-1 mice fed the iron deficient (7 ppm Fe), iron sufficient (120 ppm Fe), and high-iron diets (3000 or 5000 ppm Fe) for 54 d. The IgM and IgG antibody responses against sheep erythrocytes (SRBC) determined by hemolytic plaque assay were suppressed by 65.4 and 51.2%, respectively, in the iron deficient mice. Subclinical iron deficiency was manifested by a marked reduction in hepatic iron concentration without any changes in hematocrit or body weight gain. In contrast, consumption of high-iron diets caused a marked accumulation of iron in the liver and a twofold reduction in the IgM antibody response without alteration in the IgG response. The suppression of the IgG antibody response in the iron deficient mice, however, did not result in a compensatory increase in delayed type hypersensitivity response.

Animals↗
PubMed1995

[Transferrin receptor and iron deposition pattern in the hepatic lobules of the iron-deficient and iron-overloaded rats].

Wistar rats were made iron deficient by a low iron regimen. Iron overload was produced by repeated intraperitoneal injections of ferric nitrilotriacetate (Fe(3+)-NTA) for one to four months. Hepatic tissues from these iron deficient, overloaded and control rats were examined for transferrin receptor (TfR), transferrin (Tf) and iron after immunohistochemical staining. TfR and Tf were mainly distributed in the peripheral part of the lobule (zone 1) in the normal, iron deficient and iron-overloaded rats. The staining intensity decreased from zone 1 to zone 3. The staining intensity of TfR was strongest in iron-deficiency rat hepatic cells, weakest in iron-overloaded rat hepatic cells when compared with controls. The difference of Tf staining between the three groups of rats was similar to that of TfR. In the iron-overloaded rats, the staining intensity of iron was stronger in zone 1 than in zone 2 and 3, similar to the distribution pattern of TfR and Tf. These findings suggest that (1) iron uptake in hepatic cells in vivo is regulated and mediated by TfR and Tf, (2) the expression pattern of TfR and Tf in zone 1 to zone 3 liver cells may result in the progressive decrease of iron deposition in the hepatic lobules of the iron overloaded rats.

Anemia, Iron-Deficiency↗