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

The present study was designed to investigate the effects of nickel chloride on dietary iron deficiency in rats. The degree of iron deficiency was relatively moderate, but a more generalized anemia occurred in iron deficiency, in absence of nickel chloride. Moderate iron deficiency anemia induced increased lactate-dehydrogenase activity of serum and bone marrow, perhaps related to the decreased production of energy by oxidative means. Nickel chloride, perhaps for its ability to change iron absorption, for the maintenance of bone marrow metabolism and for to increase ceruloplasmin activity, inhibited the alteration on hemoglobin synthesis. Furthermore, nickel chloride possibly for its action on copper content and Cu-Zn superoxide-dismutase activity, inhibits the shortening of the red cell life span, caused by superoxide radicals.
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PMID:Influence of nickel chloride on iron-deficiency in rats. 263 91

Fully crossed, factorially arranged experiments showed that, under defined conditions, interactions occur between nickel and iron, nickel and copper, arsenic and zinc, and possibly vanadium and chromium. Nickel and iron interacted when dietary iron was supplemented as ferric sulfate only. Signs of nickel deprivation were more severe when dietary iron was low; or the signs of moderate iron deficiency were more severe when dietary nickel was deficient. When iron was supplemented to the diet as a 60% ferric-40% ferrous sulfate mixture, nickel and iron apparently did not interact. The findings suggested a synergistic relationship between nickel and iron when dietary iron was in a relatively unavailable form. An antagonistic interaction between nickel and copper was found when dietary iron was supplemented as a 60% ferric-40% ferrous sulfate mixture. Signs of copper deficiency were more severe in nickel-supplemented than in nickel-deprived rats. When the rats were made severely iron deficient by feeding of low levels of ferric sulfate only, no apparent interaction between nickel and copper was found. The interaction between arsenic and zinc apparently was noncompetitive. When dietary zinc was 40 microgram/g, arsenic-deprived chicks exhibited depressed growth and elevated hematocrits. In zinc deficiency, growth was more markedly depressed and hematocrits more markedly elevated in arsenic-supplemented than in arsenic-deficient chicks. Arsenic might be necessary for the efficient utilization or metabolism of zinc. Findings indicating an interaction between vanadium and chromium were tentative. In one experiment, the addition of 500 microgram of chromium/g of diet apparently made 5 micrograms of vanadium/g of diet toxic for chicks. Thus, the interactions between essential trace and ultratrace elements might be of nutritional significance.
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PMID:Interactions between essential trace and ultratrace elements. 694 Apr 72

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

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

The present investigation was designed to examine the effect of nickel deficiency on lipid metabolism in liver and serum lipoproteins of rats. Therefore, a study over two generations was conducted feeding a nickel-deficient diet containing 13 microg/kg nickel or a nickel-adequate diet supplemented with 1 mg/kg nickel. Male 7-wk-old pups from the second offspring were studied. Pups fed a diet poor in nickel tended to have lower weight gains (P < 0.15), nickel concentrations in liver (P < or = 0.1) and iron levels in serum (P < 0.1) than nickel-adequate rats. They were classified as nickel-deficient on the basis of significantly lower erythrocyte counts, hemoglobin concentrations, hematocrits and nickel concentrations in kidney compared with nickel-adequate rats. Nickel deficiency caused a significant triacylglycerol accumulation in liver, with greater concentrations of saturated fatty acids, monounsaturated fatty acids, and polyunsaturated fatty acids than nickel-adequate rats. Nickel deficiency had slight but significant effects on the fatty acid composition of liver total lipids and phosphatidylcholine and phosphatidylethanolamine. Moreover, nickel-deficient rats had significantly lower activities of the lipogenic enzymes glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, malic enzyme and fatty acid synthase than nickel-adequate rats. Nickel-depleted pups had significantly higher concentrations of triacylglycerols and phospholipids in serum VLDL, and cholesterol in serum LDL than nickel-adequate pups. Most of these alterations in lipid metabolism are similar to those obtained in several iron-deficiency studies. Because nickel deficiency also slightly compromised iron status, it is possible that at least some of the observed alterations are due to the moderate iron deficiency.
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PMID:Nickel deficiency alters liver lipid metabolism in rats. 885 6

Metal ions are essential cofactors for a wealth of biological processes, including oxidative phosphorylation, gene regulation and free-radical homeostasis. Failure to maintain appropriate levels of metal ions in humans is a feature of hereditary haemochromatosis, disorders of metal-ion deficiency, and certain neurodegenerative diseases. Despite their pivotal physiological roles, however, there is no molecular information on how metal ions are actively absorbed by mammalian cells. We have now identified a new metal-ion transporter in the rat, DCT1, which has an unusually broad substrate range that includes Fe2+, Zn2+, Mn2+, Co2+, Cd2+, Cu2+, Ni2+ and Pb2+. DCT1 mediates active transport that is proton-coupled and depends on the cell membrane potential. It is a 561-amino-acid protein with 12 putative membrane-spanning domains and is ubiquitously expressed, most notably in the proximal duodenum. DCT1 is upregulated by dietary iron deficiency, and may represent a key mediator of intestinal iron absorption. DCT1 is a member of the 'natural-resistance-associated macrophage protein' (Nramp) family and thus its properties provide insight into how these proteins confer resistance to pathogens.
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PMID:Cloning and characterization of a mammalian proton-coupled metal-ion transporter. 924 8

DMT1 has four names, transports as many as eight metals, may have four or more isoforms and carries out its transport for multiple purposes. This review is a start at sorting out these multiplicities. A G185R mutation results in diminished gastrointestinal iron uptake and decreased endosomal iron exit in microcytic mice and Belgrade rats. Comparison of mutant to normal rodents is one analytical tool. Ectopic expression is another. Antibodies that distinguish the isoforms are also useful. Two mRNA isoforms differ in the 3' UTR: +IRE DMT1 has an IRE (Iron Responsive Element) but -IRE DMT1 lacks this feature. The +/-IRE proteins differ in the distal 18 or 25 amino acid residues after shared identity for the proximal 543 residues. A major function is serving as the apical iron transporter in the lumen of the gut. The +IRE isoform appears to have that role. Another role is endosomal exit of iron. Some evidence indicts the -IRE isoform for this function. In our ectopic expression assay for metal uptake, four metals--Fe2+, Mn2+, Ni2+ and Co2+--respond to the normal DMT1 cDNA but not the G185R mutant. Two metals did not--Cd2+ and Zn2+--and two--Cu2+ and Pb2+--remain to be tested. In competition experiments in the same assay, Cd2+, Cu2+ and Pb2+ inhibit Mn2+ uptake but Zn2+ did not. In rodent mutants, Fe and Mn appear more dependent on DMT1 than Cu and Zn. Experiments based on ectopic expression, specific antibodies that inhibit metal uptake and labeling data indicate that Fe3+ uptake depends on a different pathway in multiple cells. Two isoforms localize differently in a number of cell types. Unexpectedly, the -IRE isoform is in the nuclei of cells with neuronal properties. While the function of -IRE DMT1 in the nucleus is speculative, one may safely infer that this localization identifies new role(s) for this multifunctional transporter. Management of toxic challenges is another function related to metal homeostasis. Airways represent a gateway tissue for metal entry. Preliminary evidence using specific PCR primers and antibodies specific to the two isoforms indicates that -IRE mRNA and protein increase in response to exposure to metal in lungs and in a cell culture model; the +IRE form is unresponsive. Thus the -IRE form could be part of a detoxification system in which +IRE DMT1 does not participate. How does iron status affect other metals' toxicity? In the case of Mn, iron deficiency may enhance cellular responses.
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PMID:DMT1: a mammalian transporter for multiple metals. 1257 63

Iron acquisition in Arabidopsis depends mainly on AtIRT1, a Fe2+ transporter in the plasma membrane of root cells. However, substrate specificity of AtIRT1 is low, leading to an excess accumulation of other transition metals in iron-deficient plants. In the present study we describe AtIREG2 as a nickel transporter at the vacuolar membrane that counterbalances the low substrate specificity of AtIRT1 and possibly other iron transport systems in iron-deficient root cells. AtIREG2 is co-regulated with AtIRT1 by the transcription factor FRU/FIT1, encodes a membrane protein, which has 10 putative transmembrane domains and shares homology with vertebrate Fe2+ exporters. Heterologous expression of AtIREG2 in various yeast mutants, however, did not demonstrate an iron transport function. Instead, expression in wild-type and nickel-sensitive cot1 yeast cells conferred enhanced tolerance to elevated concentrations of nickel at acidic pH. A role in vacuolar substrate transport was further supported by localization of AtIREG2-GFP fusion proteins to the tonoplast in Arabidopsis suspension cells and root cells of intact plants. Transgenic plants overexpressing AtIREG2 showed an increased tolerance to elevated concentrations of nickel, whereas T-DNA insertion lines lacking AtIREG2 expression were more sensitive to nickel, particularly under iron deficiency, and accumulated less nickel in roots. We therefore propose a role of AtIREG2 in vacuolar loading of nickel under iron deficiency and thus identify it as a novel component in the iron deficiency stress response.
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PMID:AtIREG2 encodes a tonoplast transport protein involved in iron-dependent nickel detoxification in Arabidopsis thaliana roots. 1679 Apr 30

Networks of transcription factors control physiological, developmental and environmental responses. Root iron acquisition responses are controlled by the essential bHLH protein FIT. Recently, two group Ib BHLH genes were reported to be iron deficiency-regulated. Here, we studied expression patterns of these two group Ib BHLH genes and of their two closest homologs to analyze whether their regulation would support a function in iron deficiency responses. We found that BHLH038, BHLH039, BHLH100 and BHLH101 (comprising a subgroup of BHLH Ib genes) were up regulated by iron deficiency in roots and leaves. Single insertion mutants had no visible phenotype and were capable of inducing root iron acquisition responses, presumably due to functional redundancy. Specific metal treatments like nickel, high zinc or high copper resulted in induction of the four BHLH Ib genes whereas high iron, low copper and low zinc repressed gene expression. Induction of the four BHLH Ib genes was also found in multiple iron acquisition mutants including fit. Ectopic activation of FIT did not suppress the four BHLH Ib genes. Split-root analyses using promoter-GUS lines showed that FIT and BHLH100 promoters were controlled by different local and systemic signals involved in their regulation by iron. These results indicated that the four BHLH Ib genes were induced independently from FIT by conditions causing iron deficiency. Taken together, BHLH038, BHLH039, BHLH100 and BHLH101 function differently from FIT and may be involved in mediating a signal related to iron deficiency-induced stress and/or internal iron homeostasis.
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PMID:Iron deficiency-mediated stress regulation of four subgroup Ib BHLH genes in Arabidopsis thaliana. 1751 80

Nicotianamine (NA) is a non-protein amino acid derivative synthesized from S-adenosyl L-methionine able to bind several metal ions such as iron, copper, manganese, zinc, or nickel. In plants, NA appears to be involved in iron availability and is essential for the plant to complete its biological cycle. In graminaceous plants, NA is also the precursor in the biosynthesis of phytosiderophores. Arabidopsis lines accumulating 4- and 100-fold more NA than wild-type plants were used in order to evaluate the impact of such an NA overaccumulation on iron homeostasis. The expression of iron-regulated genes including the IRT1/FRO2 iron uptake system is highly induced at the transcript level under both iron-sufficient and iron-deficient conditions. Nevertheless, NA overaccumulation does not interfere with the iron uptake mechanisms since the iron levels are similar in the NA-overaccumulating line and wild-type plants in both roots and leaves under both sufficient and deficient conditions. This observation also suggests that the translocation of iron from the root to the shoot is not affected in the NA-overaccumulating line. However, NA overaccumulation triggers an enhanced sensitivity to iron starvation, associated with a decrease in iron availability. This study draws attention to a particular phenotype where NA in excess paradoxically leads to iron deficiency, probably because of an increase of the NA apoplastic pool sequestering iron. This finding strengthens the notion that extracellular NA in the apoplast could be a major checkpoint to control plant iron homeostasis.
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PMID:Increased sensitivity to iron deficiency in Arabidopsis thaliana overaccumulating nicotianamine. 1918 76


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