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

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

Fixation of dinitrogen by soil bacteria is catalyzed by the enzyme nitrogenase which requires iron, molybdenum, and/or vanadium as metal cofactors. Under conditions of iron deficiency, the ubiquitous N2-fixing bacterium Azotobacter vinelandii produces azotobactin, a fluorescent pyoverdine-like compound which serves as a siderophore. Azotobatin's hydroxamate, catechol, and alpha-hydroxy-acid moieties endow it with a very high affinity for Fe(III), and the Fe complex is taken up by the bacterium. Here we show that azotobactin also serves for the uptake of Mo and V. Azotobactin forms strong complexes with molybdate and vanadate and the complexes are taken up by regulated transport systems. The kinetics of complexation of molybdate and vanadate by azotobactin are faster than the complexation of Fe(III), which is either precipitated or bound to strong complexing agents. As a result of this kinetic advantage, the Mo and V complexes of azotobactin form despite the higher affinity of the compound for Fe, which is present in large excess in the environment. The results obtained here for azotobactin and previous data for the bis- and tris-catechols produced by A. vinelandii show that those "siderophores" are really "metallophores" that promote the bacterial acquisition of Mo and V in addition to Fe.
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PMID:Role of the siderophore azotobactin in the bacterial acquisition of nitrogenase metal cofactors. 1984 25

Oligodendrocyte development and myelination occurs vigorously during the early post natal period which coincides with the period of peak mobilization of iron. Oligodendrocyte progenitor cells (OPCs) are easily disturbed by any agent that affects iron homeostasis and its assimilation into these cells. Environmental exposure to vanadium, a transition metal can disrupt this iron homeostasis. We investigated the interaction of iron deficiency and vanadium exposure on the myelination infrastructure and its related neurobehavioural phenotypes, and neurocellular profiles in developing rat brains. Control group (C) dams were fed normal diet while Group 2 (V) dams were fed normal diet and pups were injected with 3mg/kg body weight of sodium metavanadate daily from postnatal day (PND) 1-21. Group 3 (I+V) dams were fed iron deficient diet after delivery and pups injected with 3mg/kg body weight sodium metavanadate from PND1-21. Body and brain weights deteriorated in I+V relative to C and V while neurobehavioral deficit occurred more in V. Whereas immunohistochemical staining shows more astrogliosis and microgliosis indicative of neuroinflammation in I+V, more intense OPCs depletion and hypomyelination were seen in the V, and this was partially protected in I+V. In in vitro studies, vanadium induced glial cells toxicity was partially protected only at the LD 50 dose with the iron chelator, desferroxamine. The data indicate that vanadium promotes myelin damage and iron deficiency in combination with vanadium partially protects this neurotoxicological effects of vanadium.
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PMID:The Deterioration Seen in Myelin Related Morphophysiology in Vanadium Exposed Rats is Partially Protected by Concurrent Iron Deficiency. 2757 59