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

The nature of riboflavin precursors was studied in the yeast Pichia guilliermondii. By means of mutants with blocked GMP-synthetase the purine precursors of riboflavin were shown to belong to guanylic compounds. Accumulation of 2,4,5-triamino-6-oxypyrimidine, 2,5-diamino-6-oxy-4-ribitylaminopyrimidine, 2,6-dioxy-5-amino-4-ribitylaminopyrimidine (DOARAP) and 6,7-dimethyl-8-ribityllumasine occurs in the riboflavin-deficient mutants divided into five biochemical groups. This fact evidences for identity of riboflavin precursors in the yeast P. guilliermondii and Saccharomyces cerevisiae. Synthesis of DOARAP by the washed off cells of the mutants with the blocked lumasine synthetase is strongly inhibited by riboflavin; cycloheximide in the absence of riboflavin has no effect on this process. Consequently, flavinogenesis in P. guilliermondii is regulated according to the type of negative feedback by means of retroinhibition mechanism. A change in the content of flavins in the cells has no effect on synthesis of riboflavin synthetase; at the same time iron deficiency in the cells evokes derepression of this enzyme. Incubation of the cells rich in iron with o-phenantroline or alpha, alpha'-dipyridyl also causes derepression of riboflavin synthetase which is inhibited by cycloheximide. A deficiency of hem in the mutants which need epsilon-aminolevulinic acid does not affect the riboflavinsynthetase activity of the cells. Evidently, in P. guilliermondii a certain form of nonheminic iron might take part in regulating synthesis of riboflavin synthetase and other enzymes participating in riboflavin biosynthesis. Riboflavin overproduction is established to require formation of purines de novo. With the absence of flavinogenesis enzymes derepression a genetic disturbance in regulation of purinic nucleotides biosynthesis results in stimulation of flavinogenesis. The properties were studied for 680 time purified riboflavinkinase from cells of P. guilliermondii as well as for three phosphatases possessing the optimum of the activity at pH 3.5, 5.5 and 8.6, which ARE ABLE OF HYDROLYSING FMN. A change in the content of flavins and iron in the cells has no effect on the activity of riboflavinkinase in this species. Evidently, the mechanisms of riboflavin and flavin nucleotides biosynthesis regulation would be different in P. guilliermondii.
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PMID:[Biosynthesis of flavins and its regulation in the yeast Pichia guilliermondii]. 0 Aug 34

Relationships between various types of chronic anemia, wound healing, and red cell 2,3-diphosphoglycerate (2,3 DPG) were examined in rabbits. Wound tensile strength and energy absorption were not affected by chronic iron-deficiency anemia, the chronic hemolytic anemia caused by intravenous water infusion nor by chronic hemolytic anemia caused by intravenous water infusion nor by chronic phenylhydrazine-induced anemia. Red cell 2,3 DPG levels were increased in the anemia of iron deficiency and were normal in the rabbits with chronic phenylhydrazine-induced anemia at the time of wound excision but were low following phynylhydrazine injection. The results show that chronic anemia per se does not affect the tensile strength and energy adsorption of wound healing. The findings suggest that the wound healing process may differ in certain types of anemia.
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PMID:Chronic anemia, wound healing, and red cell 2,3-diphosphoglycerate. 0 66

Hemin allows maximal protein synthesis in intact rabbit reticulocytes and their cell-free lysate preparations by retarding the formation of a translational repressor (HCR) found in the postribosomal supernate. In order to evaluate the role of HCR in the pathogenesis of hypochromic anemias, HCR was isolated and partially purified from intact rabbit reticulocytes incubated in vitro with either 0.1 mM alpha,alpha-dipyridyl (an iron-chelating agent) or 0.1 M ethanol. Both of these agents inhibit reticulocyte protein synthesis. Hemin (50 muM) protects against the inhibition by both agents. A ferrous iron-transferrin mixture, however, protects only against alpha,alpha-dipyridyl. Both alpha,alpha-dipyridyl and ethanol inhibit heme synthesis before the time that protein synthesis is affected, while neither lowers either ATP or GSH levels. These results indicate that while both agents inhibit heme synthesis, alpha,alpha-dipyridyl does so by inducing iron deficiency while ethanol works at a non-iron-requiring step. When HCR was isolated from intact cells and assayed in the reticulocyte cell-free systems, plus and minus hemin, premature appearance of HCR was found in cells incubated in vitro with alpha,alpha-dipyridyl or ethanol. When hemin was present in the intact cell incubation, the appearance of HCR was retarded. The HCR from alpha,alpha-dipyridyl ethanol-treated cells was partially purified and eluted at the same location on a Sephadex G-200 column (molecular weight approximately 3 x 10(5)) as that from postribosomal supernates incubated minus hemin. In addition rabbits with phenylhydrazine-induced hemolytic anemia were given intravenous ethanol in vivo at a dose of 0.4 ml/kg. This concentration of alcohol resulted in an inhibition of the rate of heme synthesis and protein synthesis as well as an acceleration of HCR formation in reticulocytes. The HCR from these in vivo treated rabbits was isolated, partially purified, and assayed in an identical fashion as the in vitro experiments. These in vivo experiments further support the physiological and pathophysiological role of HCR in reticulocytes. On the basis of these results a model for a role of HCR in some of the hypochromic anemias is proposed. In iron deficiency or chronic disease (where iron is not available to the erythroblast for heme synthesis) HCR appears prematurely and inhibits protein synthesis. When heme synthesis is inhibited by ethanol but there is sufficient intracellular iron, HCR appears prematurely and inhibits protein synthesis, iron accumulates in the erythroblast, and the end result is sideroblastic anemia.
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PMID:A rabbit reticulocyte model for the role of hemin-controlled repressor in hypochromic anemias. 0 17

Fifty-five patients have been investigated for anaemia in pregnancy. Using the serum iron/T.I.B.C. ratio as a diagnostic index it has been found that iron deficiency exists in 60% of our expectant mothers with mild anaemia. This type of anaemia was more common in multiparous women and more frequent in the first and second trimesters of pregnancy, There is, therefore, a strong indication for the routine administration of iron supplements to our women during pregnancy and the puerperium.
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PMID:Diagnosis of iron deficiency anaemia among Nigerian pregnant women by serum iron/T.I.B.C. determination. 1 12

Chronic nutritional iron deficiency of 2 to 5 weeks duration reduced the blood hemoglobin content to 30-50% of control values and resulted in an increase in rat adrenal tyrosine hydroxylase (TH) (EC 1.14.16.2) activity. Kinetic and mixing experiments indicated that this increase was due to an increase in enzyme protein. The body weight of iron-deficient rats ranged from 60 to 80% of control; this factor, however, was not responsible for the increase in adrenal TH as enzyme activity was directly proportional to final body weight. To determine whether the increase in adrenal TH in iron-deficient rats was due to increased sympathetic activity to the adrenal medulla, the splanchnic nerve was cut. The increased TH was still observed after adrenal denervation; this indicates that the mechanism of response to iron deficiency lies within the adrenal itself. Age of the rats is important in determining whether the increase in TH activity will occur.
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PMID:The effect of chronic iron deficiency on adrenal tyrosine hydroxylase activity. 1 18

Ninety-four Nigerian pregnant women, many of who had mild to moderate anaemia, were investigated for the presence of iron deficiency. Using the bone marrow as the diagnostic index, 90% of these patients were found to be iron deficient. Iron deficiency is thus common among our expectant mothers. They should, therefore, be given iron supplement in addition to the present practice of folic acid and antimalarials, throughout pregnancy and the puerperium.
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PMID:Iron deficiency anaemia in Nigerian pregnant women. 1 99

A siderophore (microbial iron transport compound) was isolated from low iron cultures of Agrobacterium tumefaciens B6. The substance was characterized as a threonyl peptide of spermidine acylated with 3 residues of 2,3-dihydroxybenzoic acid, the carbonyl group of 1 residue of the latter participating in an oxazoline ring with the beta-hydroxyl of the threonine moiety. The compound, N-[3-(2,3-dihydroxybenzamido)propyl]-N-[4-(2,3-dihydroxybenzamido)butyl]-2-(2,3-dihydroxyphenyl)-trans-5-methyl-oxazoline-4-carboxamide, was given the trivial name agrobactin. Exposure to acid opened the oxazoline ring to afford agrobactin A. Ferric agrobactin A and agrobactin A itself, but not agrobactin or its ferric complex, had some capacity to feed iron to enterobactin-deficient strains of Escherichia coli and Salmonella typhimurium. Agrobactin was produced by A. tumefaciens in response to iron deficiency and was able to reverse the iron starvation in this organism precipitated by the presence of a ferric complexing agent not utilized by the cells.
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PMID:Agrobactin, a siderophore from Agrobacterium tumefaciens. 3 87

The daily dietary iron intake of nine pregnant Nigerian women with confirmed iron deficiency anemia was determined. The daily dietary iron intake from hospital meals served to ten other pregnant women was also assessed to serve as a control. The mean daily iron intake of the group of anemic patients on home diet was 14.6 mg (range of individual means = 8.37-25.28 mg), whereas the group of patients served hospital meals had a mean daily dietary iron intake of 36.92 mg (range of individual means = 25.09-46.47 mg). It is, therefore, clear that the etiology of iron deficiency in the patients studied was mainly dietary. Thus, our pregnant patients, many of whom are on diets similar to those of the group studied, should receive iron supplements during pregnancy.
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PMID:Dietary iron intake of pregnant Nigerian women with anemia. 4 89

3H-thymidine incorporation into normoblasts, proliferation rate of erythroid precursors and degree of intramarrow hemolysis have been studied in vitro on the bone marrow. The normal proliferation rate of normoblasts is 26 +/- 2% i.e. during 24 hours about a quarter of dividable elements of erythropoiesis is renewed. Acute blood loss increases the proliferation rate up to 57 +/- 9% but the value of 3H-thymidine incorporation into cells is not changed as compared to normal. In chronic blood loss both 3H-thymidine incorporation into dividing erythroid precursors at different stages of maturity and the rate of erythroid production are 2 to 3 times lower than normal. In healthy persons the degree of intramarrow hemolysis is 7 +/- 2% of erythroid precursors incubated for 24 hours. In iron deficiency anemia intramarrow destruction sharply increases, presenting at an average 30% of incubated nucleated elements of erythropoiesis. A type of chronic iron deficiency, which is not associated with blood loss, is described. In this type of anemia the proliferation rate of normoblasts and the degree of intramarrow hemolysis do not differ from normal values.
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PMID:Proliferative activity of erythrone and intramarrow hemolysis in iron deficiency anemias. 5 Sep 70

Nutritional anaemia is a major public-health problem in many parts of the world, and iron deficiency appears to be the most important cause. The immune response is believed to be impaired in anaemia. The results of the present study, carried out in young children, indicate that both the cell-mediated immune response and the bactericidal activity of leucocytes are impaired when levels of haemoglobin fall to 10 g/dl or less.
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PMID:Anaemia and immune response. 5 5


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