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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The chromatographic elution patterns on Sepharose 6B of the supernatant from mucosal homogenates prepared 10 min after administration of copper into duodenal segments in vivo, indicate that copper is bound preferentially in the fraction of mucosal transferrin. 2. In iron deficiency the amount of 64Cu-copper taken up into the duodenal mucosa is more than two times higher and the amount bound to proteins of the supernatant is also increased to approximately the same degree whereas the amount transferred into the body is diminished to one fourth. 3. In the iron deficient group 64Cu-copper was also bound to a fraction which contains probably metallothionein. 4. The distribution of copper in the supernatant was changed due to a simultaneous administration of iron; the amount of copper bound in the transferrin fraction decreased in favor of the metallothionein fraction and another copper binding fraction was eluted between the transferrin and the metallothionein fraction. 5. Copper in a tenfold molar excess inhibited the iron absorption; simultaneously, the iron bound in the iron binding fractions of the supernatant was remarkably diminished. 6. The results suggest that the affinity of copper to two mucosal iron binding proteins, transferrin and metallothionein, is at least partly responsible for the inhibitory effect of copper on iron absorption in iron deficiency.
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PMID:Binding of copper to mucosal transferrin and inhibition of intestinal iron absorption in rats. 42 57

The interaction of dietary iron and zinc was studied in chicks. Zinc was found to be more toxic in iron-deficient animals than iron-supplemented animals as measured by hemoglobin concentrations and growth. Analyses of the kidney and liver for iron and zinc were carried out. As the level of iron was increased from 0-1000 ppm supplementation, the concentration of liver zinc increased. The organ levels of iron were decreased as the dietary zinc levels were increased from 0-5000 ppm. Radioisotope studies using 65Zn revealed that the iron content of the diet did not affect absorption of zinc. Administration of the isotope, either in an intestinal segment or intravenously, resulted in more zinc being taken up by the liver in the iron supplemented animals. This was especially noted when the ratio of the isotope in liver to that in the blood was compared. Gel chromatography of kidney and liver homogenates revealed that iron deficiency resulted in less zinc being eluted in a volume characteristic of metallothionein compared to homogenates of organs from iron supplemented animals. The results indicate that iron-supplemented animals have a greater capacity for sequestering zinc on metallothionein than do iron-deficient animals. Conversely, iron-deficient chicks were more susceptible to the effects of zinc toxicity than are iron-adequate chicks.
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PMID:Studies on the role of iron in zinc toxicity in chicks. 248 56

Studies were conducted to determine the effect of dietary iron (Fe) levels ranging from a deficiency to an excess on the toxicity of cadmium (Cd) in chicks. In Fe-deficient animals, cadmium was found to be more toxic than in Fe supplemented animals as measured by growth. The liver Cd burdens were increased significantly in the presence of dietary Fe supplementation, and there was a significant Cd-Fe interaction in the Cd concentration of the kidney, indicating that iron deficiency increased the concentration of Cd in the kidneys of those chicks receiving this element. Cd tended to reduce the Fe concentration in both the liver and kidney. The absorption of Cd as measured by the amount of 109Cd that disappeared from an isolated duodenal segment in one h was not affected by the Fe content of the diet, but the amount of isotope appearing in the liver compared to the amount present in the blood was increased in the Fe supplemented chicks. Separation of the Cd binding ligands by column chromatography revealed that more of the Cd in the liver, but not the kidney, was associated with ligands which eluted in a column volume that contained metallothionein in those chicks receiving Fe than in the livers from Fe deficient animals. The inverse relationship between the amount of Cd bound to the metallothionein containing fraction and toxicity may be related causally.
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PMID:Studies on the role of iron in the reversal of cadmium toxicity in chicks. 248 63

The effects of iron deficiency and of restriction of food intake on blood and tissue metallothionein-I (MT-I) concentrations in rats were investigated. Compared to ad libitum fed controls, MT-I concentrations in the blood cells of the iron-deficient rats were higher, whereas concentrations in pair-fed control rats were lower. Iron deficiency also increased MT-I concentrations in the bone marrow but concentrations in the liver were unchanged and those in the kidneys were reduced. The MT-I in the blood cells was associated mainly with the lighter cell fractions which were rich in reticulocytes. It is suggested that concentrations of MT-I in blood cells reflect erythropoietic activity.
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PMID:Effects of iron deficiency on metallothionein-I concentrations in blood and tissues of rats. 292 43

Effects of cadmium (Cd) on in vitro and in vivo erythropoiesis in rats were studied by methylcellulose colony assay. Cd suppressed the in vitro growth of late erythroid progenitors (CFU-E) in a dose-dependent fashion and did not lose its inhibitory potency with increasing doses of erythropoietin (EPO). In addition, in marrow suspension cultures, Cd did not significantly influence 59Fe incorporation into both the cells and heme, and the Cd dose-responsive inhibition curve of the number of living cells was similar to that of CFU-E. These results suggest that the suppression of CFU-E colony formation by Cd is not due to the blocking of either EPO action to stimulate the growth of CFU-E or the iron incorporation into the cells ahd heme, but due to its direct cytotoxic effect. The colony suppression by Cd could be prevented by adding metallothionein to the cultures. On the other hand, oral administration of Cd to animals (100 mg/liter in drinking water) induced an iron deficiency anemia characterized by microcytic hypochromic red cells, decreased plasma iron, and increased total iron binding capacity. Marrow CFU-E density steadily increased as plasma iron decreased due to Cd administration and reached a plateau after 50 days. Plasma EPO titers were also found to be elevated in such a Cd-induced anemia. Parenteral iron administration during the Cd drinking period could completely prevent the development of iron deficiency anemia and the increase of both CFU-E and plasma EPO. There was a hyperbolic correlation between CFU-E and plasma iron or transferrin saturation. These results demonstrate that oral CD administration produces bone marrow hyperplasia at the CFU-E level due to iron deficiency.
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PMID:Effects of cadmium on in vitro and in vivo erythropoiesis: erythroid progenitor cells (CFU-E), iron, and erythropoietin in cadmium-induced iron deficiency anemia. 339 Dec 51

Lead, cadmium, and mercury are toxic metals that are not essential for nutrition. However, the toxic effects of these metals may be mediated or enhanced by interactions or deficiencies of nutritionally essential metals. Lead competes with calcium, inhibiting the release of neurotransmitters, and interferes with the regulation of cell metabolism by binding to second-messenger calcium receptors, blocking calcium transport by calcium channels and calcium-sodium ATP pumps, and by competing for calcium-binding protein sites and uptake by mitochondria. Dietary deficiencies of calcium, iron, and zinc enhance the effects of lead on cognitive and behavioral development. Iron deficiency increases the gastrointestinal absorption of cadmium, and cadmium competes with zinc for binding sites on metallothionein, which is important in the storage and transport of zinc during development. Selenium protects from mercury and methyl mercury toxicity by preventing damage from free radicals or by forming inactive selenium mercury complexes.
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PMID:Nutrition and metal toxicity. 787 32

The influence of dietary iron deficiency on acute nickel, lead or cadmium toxicity as reflected by the induction of hepatic, renal, and intestinal metallothionein (MT), disposition of the metals and alterations in hematological parameters, was investigated in young rats to ascertain whether the toxic effects of these metals modify under anemic conditions. The administration of Cd induced hepatic, renal and intestinal MT while that of Ni or Pb induced hepatic MT only. While dietary Fe deficiency did not affect MT induction by Cd, it enhanced the synthesis of renal and intestinal MT by Ni and Pb. The accumulation of Pb in liver and kidney and that of Cd in liver only, were enhanced by Fe deficiency; the tissue deposition of Ni remained unaffected by Fe deficiency. The induction of hepatic MT by Ni, Pb or Cd appears to be related to the concomitant rise in the hepatic Zn, Ca and Fe levels in normal rats. However, dietary Fe deficiency increased the hepatic Zn in response to Ni or Cd and the hepatic Ca in response to Pb administration.
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PMID:Influence of dietary iron deficiency on nickel, lead and cadmium intoxication. 802 92

A lambda zapII cDNA library was constructed from mRNA isolated from Fe-deficient barley roots and screened with cDNA probes made from mRNA of Fe-deficient and Fe-sufficient (control) barley roots. Seven clones were selected. Among them a clone having the putative full-length mRNA of dioxygenase as judged by northern hybridization was selected and named Ids2 (iron deficiency-specific clone 2). Using a cDNA fragment as probe, two clones from the genomic library (lambda EMBL-III) were isolated and one was sequenced. The predicted amino acid sequence of Ids2 resembled that of 2-oxoglutarate-dependent dioxygenase. Ids2 is expressed in the Fe-deficient barley roots but is not in the leaves. The expression is repressed by the availability of Fe. Ids2 was also strongly expressed under Mn deficiency and weakly under Zn deficiency or excess NaCl (0.5%). The upstream 5'-flanking region of Ids2 has a root-specific cis element of the CaMV 35S promoter and a nodule-specific element of leghemoglobin, a metal regulatory element (MRE) and several Cu regulatory elements (UAS) of yeast metallothionein (CUP1).
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PMID:A dioxygenase gene (Ids2) expressed under iron deficiency conditions in the roots of Hordeum vulgare. 806 21

The influence of dietary iron deficiency on acute nickel, lead or cadmium toxicity as reflected by the induction of hepatic, renal and intestinal metallothionein (MT), disposition of the metals, and alterations in hematological parameters was investigated in rats. The administration of cadmium induced the hepatic, renal and intestinal MT while that of nickel or lead induced hepatic MT only. However, dietary iron deficiency did not influence the cadmium induced tissue MT but enhanced the ability of nickel or lead to restore the normal synthesis of renal and intestinal MT lowered under the influence of reduced body iron status. The accumulation of lead in liver and kidney and that of cadmium enhanced in liver only, while tissue deposition of nickel remained unaffected by iron deficiency. The induction of hepatic MT by three metals appears related to the concomitant rise in the hepatic zinc, calcium and iron levels in normal rats. However, dietary iron deficiency increased the hepatic zinc in response to nickel or cadmium and that of heptic calcium in response to lead.
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PMID:Influence of dietary iron deficiency on acute metal intoxication. 835 7

Transferrin, metallothionein, cytochrome P-450, and the in vitro formation of DNA-benzo[a]pyrene adducts were studied in the offspring of dams that were fed diets moderately or severely deficient in iron (Fe). The study was designed to determine whether Fe deficiency-induced alterations were reversible or if they persisted with post-weaning iron repletion. Throughout gestation and lactation the dams were fed a Control diet = 120 micrograms Fe/g diet, a Marginal Iron diet = 11 micrograms Fe/g diet, or a Low Iron diet = 7 micrograms Fe/g diet. On day 14 of lactation, 4 pups per litter were killed. On day 21, the dams were killed. Half of the remaining pups in each litter were fed their respective diets until they were killed on day 42 (Marginal Iron-Marginal Iron and Low Iron-Low Iron groups). The other half were fed the Control diet (Marginal Iron-Control and Low Iron-Control groups). The dietary intake of the Restricted Fed offspring was matched to rats in the Low Iron-Low Iron group. Offspring in the iron-deficient groups had hematocrits, hemoglobin concentrations, and liver iron levels that were lower than Controls. Day 42 offspring in the iron-deficiency groups had a lower food intake and higher liver zinc and copper levels than Controls. Day 14 Marginal and Low Iron pups had liver metallothionein levels that were lower than Controls. Day 42 Restricted Fed offspring had liver metallothionein levels that were higher than all other groups. Cytochrome P-450 levels and the in vitro formation of benzo[a]pyrene-DNA adducts were higher in Low Iron-Low Iron males than in Control males. Ethoxycoumarin O-deethylase activity was higher in day 42 Low Iron-Low Iron offspring than in Controls. These results show that the iron deficiency-induced alterations were transient, reversible with iron repletion, and in the case of cytochrome P-450 and ethoxycoumarin O-deethylase activity, dependent on the age and sex of the animal.
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PMID:Effects of marginal and severe iron deficiency on hepatic proteins in developing rats are reversible with dietary iron repletion. 844 18


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