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

Iron supplements are commonly administered to infants in order to prevent iron deficiency. We wished to determine whether iron administration could compromise zinc nutrition as might be suspected from previous studies. Measures of iron nutrition, serum zinc, and serum copper were measured before and after randomization of 291 healthy 1-yr-old infants to a 3 mo course of placebo or iron treatment (30 mg iron as ferrous sulfate given before a meal). There was no significant difference in serum zinc or copper in the two groups before or after treatment; thus iron administration did not result in any evidence of zinc deficiency in a healthy, well-nourished group of T-yr-old infants.
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PMID:Does iron supplementation compromise zinc nutrition in healthy infants? 405 Jul 28

The importance of ceruloplasmin in iron metabolism was studied in swine made hypoceruloplasminemic by copper deprivation. When the plasma ceruloplasmin level fell below 1% of normal, cell-to-plasma iron flow became sufficiently impaired to cause hypoferremia, even though total body iron stores were normal. When ceruloplasmin was administered to such animals, plasma iron increased immediately and continued to rise at a rate proportional to the logarithm of the ceruloplasmin dose. The administration of inorganic copper induced increases in plasma iron only after ceruloplasmin appeared in the circulation. Thus, ceruloplasmin appeared to be essential to the normal movement of iron from cells to plasma. Studies designed to define the mechanism of action of ceruloplasmin were based on the in vitro observation that ceruloplasmin behaves as an enzyme (ferroxidase) that catalyzes oxidation of ferrous iron. Retention of injected ferrous iron in the plasma of ceruloplasmin-deficient swine was significantly less than that of ferric iron, reflecting impaired transferrin iron binding. Rat ceruloplasmin, which has little ferroxidase activity, was much less effective than porcine or human ceruloplasmin in inducing increases in plasma iron. These observations suggest that ceruloplasmin acts by virtue of its ferroxidase activity. Eight patients with Wilson's disease were evaluated in order to investigate iron metabolism in a disorder characterized by reduced ceruloplasmin levels. Evidence of iron deficiency was found in six of these, and in five of the six, plasma ceruloplasmin was less than 5% of normal. In comparison, the two patients without evidence of iron deficiency had ceruloplasmin levels of 11 and 18% of normal. It is suggested that iron deficiency tends to occur in those patients with Wilson's disease who have the severest degrees of hypoceruloplasminemia, possibly because of defective transfer of iron from intestinal mucosal cells to plasma.
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PMID:The role of ceruloplasmin in iron metabolism. 548 Aug 64

Both iron and copper play critical biochemical roles in the post-translational modifications of collagen and elastin. These modifications are essential to the maturation and structural integrity of these proteins. Iron functions in the hydroxylation of specific prolyl and lysyl residues in collagen, a process that must occur before the triple helix can form and be extruded from the cell. Copper functions in the oxidative deamination of specific lysyl residues in the soluble forms of both elastin and collagen. This process is essential for crosslink formation and the structural integrity of these proteins. While there is no evidence that nutritional iron deficiency results in connective tissue pathology, copper deficiency impairs crosslink formation and results in gross pathology of bones, lungs and the cardiovascular system of many animal species.
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PMID:Roles for iron and copper in connective tissue biosynthesis. 611 3

Severe copper deficiency was induced in rats by rearing nursing dams and their offsprings on a semisynthetic diet comprising all the requisite nutrients and trace metals except copper. The copper-deprived rats exhibited growth retardation, severe anaemia, loss of caeruloplasmin, decrease of cytochrome oxidase, accumulation of salt-soluble collagen and a drastic decrease in iron in plasma and liver. Apart from these characteristic signs of deficiency, a marked inhibition of protein synthesis was found to occur both in vivo and in cell-free liver preparations. The curtailed ability to carry out endogenously coded amino acid incorporation into protein contrasted with the unimpaired poly(U)-acid-directed phenylalanine polymerization. This inhibition pattern, as well as the attendant disaggregation of the liver polyribosomes, suggested that the primary biosynthetic lesion was located at the stage of peptide-chain initiation. Concurrently with this alteration there was a pronounced depletion of the hepatic ATP content, associated with a parallel depression of mitochondrial respiration and an enhancement of ATPase activity. Supplementation of the copper-deficient diet with a 2-4-fold excess of iron (relative to the standard diet) prevented growth retardation and anaemia and restored normal energy metabolism, as well as unimpaired protein-synthesizing capacity. The conclusion that these disturbances were primarily determined by the secondary iron deficiency was also borne out by the finding that similar alterations occurred in rats maintained on a copper-sufficient but iron-deficient diet. On the other hand, the iron-fortified diet failed to reverse the other signs of copper deficiency, namely the loss of caeruloplasmin, the diminished rate of cytochrome oxidase and the increase of soluble collagen. The interrelations between the various biochemical lesions induced by deprivation of copper or iron are discussed and the possible role of ATP depletion in determining the derangement of protein synthesis is considered.
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PMID:Biochemical lesions in copper-deficient rats caused by secondary iron deficiency. Derangement of protein synthesis and impairment of energy metabolism. 625 58

Groups of rats were fed diets providing 8 ppm iron (-Fe) and 250 ppm iron (+Fe) throughout pregnancy and lactation. In spite of the increase in apparent absorption of iron in pregnant -Fe dams, iron deficiency anemia developed, resulting in decreased iron levels in placenta, amniotic fluid and fetal liver. Copper concentration of amniotic fluid was elevated in -Fe dams. On day 17 of lactation, -Fe dams and their suckling pups had hematologic evidence of iron deficiency. While liver and spleen iron decreased in 17-day-old pups, levels of copper increased. Subcellularly, the greatest increase in hepatic copper in -Fe pups was found in the cytosol, thus the increased copper deposition is not similar to copper loading. Serum ceruloplasmin activity was significantly elevated in -Fe lactating dams and was slightly, but not significantly, increased in -Fe pregnant dams and suckling pups.
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PMID:Copper metabolism in iron-deficient maternal and neonatal rats. 669 92

Two patients with long-standing nephrotic syndrome are described in whom urinary iron losses may have contributed towards an iron deficiency state. Seven other nephrotic patients were also studied. Increased urinary iron excretion was found in six out of nine patients and increased urinary copper excretion in all eight patients in whom it was measured. Trace metal losses in the urine in nephrotics may be important clinically.
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PMID:Urinary iron loss in the nephrotic syndrome--an unusual cause of iron deficiency with a note on urinary copper losses. 670 43

The effect of deficiency in sulfur, copper and iron in the growth medium on cyanide resistant respiration and cytochrome composition was studied in Pseudomonas aeruginosa and Candida lipolytica. It has been shown that: cyanide resistant respiration was observed at the stationary growth phase when the two microorganisms were cultivated in a complete medium; this respiration was detected already at the phase of decelerated growth in the case of copper deficiency; iron deficiency inhibited cyanide resistant respiration in the bacterium but stimulated its appearance in the yeast; sulfur deficiency inhibited the manifestation of cyanide resistant respiration in the both microorganisms; limitation of the bacterial growth with iron resulted in the accumulation of an iron complex (identical to pyoverdin in its spectral characteristics) in the cultural broth; the deficiency of sulfur, copper and iron inhibited the synthesis of all cytochromes in the bacterium; copper deficiency inhibited only the synthesis of a + a3 in the yeast; iron deficiency inhibited the synthesis of all cytochromes in the yeast; sulfur deficiency had virtually no effect on the content of cytochromes in the yeast. A possible nature of cyanide resistant oxidases in these microorganisms is discussed.
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PMID:[Effect of sulfur, copper, and iron deficiency on the development of cyanide resistant respiration and the cytochrome composition of Pseudomonas aeruginosa]. 677 39

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 content of the microelements (ME) iron, copper and zinc was determined in healthy subjects and patients with iron deficiency anemia (IDA), aged 17 to 86, subdivided into three groups: First group--51 healthy females with iron, copper and zinc levels, close to those reported in literature, the same values used for the control groups. The second group--61 females with IDA had mean copper value higher than the control norms and those of the other authors--23,842 mumol/l (151.48 mkg%). Zinc content in serum was lower than the norm. A parallel determination of serum iron was performed according to Beta-phenantroline method and AAC method with affirmative aim. The IDA group were distributed into three subgroups, depending on the causes, leading to iron deficiency: First subgroup--28 patients with undistinguished cause of iron deficiency: Second subgroup--19 patients with diseases, causing acute and chronic blood losses. Third subgroup--14 patients with various diseases (inflammatory diseases, states after difficult operations, hemopathies, etc.) without blood loss. Low serum iron was found in the three subgroups, determined according to both methods and high ISC. Serum copper level was high in the first and second subgroups, being highest in some patients with uterine myoma and gastric polyps. Serum zinc level was decreased in the second and third subgroups. The normal values of zinc in the serum of the first subgroup were associated with the absence of blood loss. Zinc is recommended to be added to the treatment of IDA.
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PMID:[Iron, copper and zinc content in healthy persons and iron-deficiency anemia patients]. 733 2

To study the effects of iron nutriture on tissue iron, copper and zinc contents, we fed iron-deficient or control diets to pregnant rats and their offspring. Pups were weaned to the same or opposite diet as that fed to their dams, yielding four groups: control-control (CC), control-deficient (CD), deficient-control (DC) and deficient-deficient (DD). Offspring were killed at 2, 21, 30, 60 and 90 days of age. Iron deficiency, induced by feeding a 5 ppm iron diet to the dam and/or to the weanlings, resulted in impaired body growth, lower hemoglobin and hematocrit levels and reduced iron levels in liver, spleen and kidney of the offspring. Two-day-old iron-deficient pups had hepatic copper levels 1.5- fold higher than control pups. By the end of the suckling period, hepatic copper levels in iron-deficient pups were 3-fold greater than those of control pups. Hepatic copper concentration in control-fed rats (CC and DC) declined with maturation. In deficient rats (CD and DD), this normal decrease in hepatic copper did not occur and in CD rats, there was a progressive accumulation of copper in the liver. Renal zinc concentrations were lower in CD and DD than in control-fed animals at 60 and 90 days of age. These interactions among iron, copper and zinc may assume clinical importance since iron deficiency is a common nutritional problem.
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PMID:Tissue iron, copper and zinc levels in offspring of iron-sufficient and iron-deficient rats. 746 70


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