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

Studies with Euglena gracilis and HL-60 cells have assessed the need for intracellular iron in the mechanisms of inhibition of cell growth and DNA damage by H2O2 and bleomycin. Cell culture media were directly depleted of iron in order to deprive cells of nutrient iron. Major pools of cellular iron were reduced in both cell types. Nevertheless, iron bound in e.s.r.-observable haem protein and ribonucleotide diphosphate reductase in HL-60 cells was not decreased. In both control cell populations, there was a concentration-dependent reduction in proliferation and cell survival caused by H2O2. In comparison, the proliferation rates of both iron-deficient cell types were significantly less sensitive to H2O2. H2O2 caused concentration-dependent single-strand breakage in DNA in control HL-60 and Euglena gracilis cells. Iron deficiency reduced the amount of strand breaks in HL-60 cells at each concentration of H2O2 used. Single-strand breakage caused by H2O2 in Euglena gracilis was a direct function of the concentration of iron in which the cells had been grown. Growth inhibition and both single- and double-strand DNA damage caused by bleomycin were substantially reduced or eliminated in iron-deficient cells. Copper bleomycin behaved like metal-free bleomycin when assayed for the capacity to cause DNA damage in iron-normal and iron-deficient HL-60 cells. In contrast, iron bleomycin was equally active under the two conditions in these cells.
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PMID:Iron requirement for cellular DNA damage and growth inhibition by hydrogen peroxide and bleomycin. 752 74

Microcytosis is common in dogs with congenital portosystemic shunts (PSS) and acquired liver disease. The objective of this study was to determine if microcytosis could be induced in normal dogs by surgical creation of PSS, and to characterize the changes in hematology and iron status. Hematocrit, mean cell volume, mean cell hemoglobin, and mean cell hemoglobin concentration decreased linearly from 45.5%, 69.1 fL, 22.8 g/dL and 33.1% to 39.5%, 55.9 fL, 17.8 g/dL and 31.9%, respectively, 18 weeks after creation of PSS. The erythrocyte count did not change, but red cell distribution widths indicated a shift to a heterogenous population with decreased volume. Mean cell volume and mean cell hemoglobin decreased rapidly after induction of PSS and were significantly (P < .05) different from presurgery values within 2 weeks. Serum iron and copper concentrations and total iron binding capacity were decreased in dogs with PSS. Liver iron concentration doubled after creation of PSS, with the majority of stainable iron located in Kupffer cells. The changes in erythrocyte indices and measures of iron status in dogs with surgically induced PSS were similar to those in dogs with congenital PSS. Microcystosis developed rapidly in dogs after induction of PSS. These results indicate that iron deficiency was not the cause of microcytosis in these dogs.
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PMID:Microcytosis and iron status in dogs with surgically induced portosystemic shunts. 806 57

Trace element concentrations in serum and breast milk were studied longitudinally in 197 Nigerian women from 6 months of gestation to 6 months postpartum; 99 of them received a daily iron supplement of 100 mg from 6 months of gestation to delivery. During the last 3 months of pregnancy, serum selenium declined, whereas serum zinc remained unchanged and serum copper increased. After delivery, copper concentration in maternal serum decreased, whereas serum zinc increased from delivery to 3 months postpartum and then reached a plateau. Serum selenium increased from delivery to 6 months postpartum. In breast milk, selenium and zinc decreased from 5 days to 6 months postpartum. Copper in breast milk also declined during the course of lactation but reached a plateau by 3 months postpartum. Iron concentration in breast milk remained unchanged during the study. Iron supplementation had no significant effect upon the concentrations of copper, selenium and zinc in mother serum and breast milk. In umbilical serum, iron status, copper and zinc levels were similar in the two groups, whereas, unexpectedly, selenium concentration was significantly decreased (p < 0.03) in the iron-supplemented group. Taken together, our results suggest that the beneficial effect of iron supplementation on iron deficiency was not associated with an adverse effect on copper and zinc status. On the other hand, our results suggest that Nigerian women had a marginal zinc status but an adequate selenium status.
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PMID:Effect of iron supplementation during pregnancy on trace element (Cu, Se, Zn) concentrations in serum and breast milk from Nigerian women. 831 20

Anaemia was detected in housed lambs by clinical and haematological investigation. Conjunctival pallor was used as a clinical test for anaemia and the results indicate that this has high specificity (91 per cent to 95 per cent) and low sensitivity (53 per cent to 55 per cent). The haematological results indicated a non-regenerative anaemia with low packed cell volume, red blood cell count and haemoglobin. In a subset of lambs examined biochemically, anaemia was associated with low serum iron concentration and low serum iron binding: cobalt levels were within normal ranges and blood copper levels were slightly raised. At present it is unclear whether this is a primary or secondary iron deficiency.
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PMID:Anaemia in housed lambs. 833 79

Rats (Wistar, female, 4 weeks old) were fed iron-deficient (Fe-; 2.2 micrograms Fe/g) or manganese- and copper-deficient (Mn.Cu-; 0.3 microgram Mn/g, 0.4 microgram Cu/g) diets for 8 weeks to determine the oxidative damage of DNA by element deficiency. After feeding of the diets, 2-nitropropane (2-NP, 80 mg/kg body weight) was administered i.p. as an inducer of 8-hydroxy-2'-deoxyguanosine (8-OH-dG) to the element-deficient rats. The hemoglobin concentration of rats in the Fe- group showed an induction of severe anemia (8.4 g/100 ml whole blood). In the Mn.Cu- group, Mn-superoxide dismutase (SOD) activities of plasma and Cu.Zn-SOD activities were significantly lower than that of the normal diet group. However, total SOD activities of plasma were not depressed severely in contrast to that of the liver in the Mn.Cu- group. Background (spontaneous) levels of 8-OH-dG in normal diet group were 0.96 +/- 0.37/10(5) deoxyguanosine (dG), however, significantly higher levels were detected in the Fe- group (1.56 +/- 0.19, P < 0.01). Conversely, a lower (but not significant) level of 8-OH-dG than the normal diet group were detected in the Mn.Cu- group (0.78 +/- 0.08). Six hours after 2-NP treatment, 8-OH-dG levels in liver DNA were significantly induced to 1.44 +/- 0.24 in the normal diet fed group 1.89 +/- 0.22 in the Fe- and 1.08 +/- 0.12 in the Mn.Cu- groups. Compared to the normal diet group, these induced levels of 8-OH-dG in the Fe- group were significantly higher (P < 0.05), and that in Mn.Cu- group were significantly lower (P < 0.05). The high level of 8-OH-dG in severe iron deficiency might be the results of: (i) an increase of hydroxyl radical generation by accumulated copper in hepatocytes; or (ii), a depression of enzymatic activity for removing 8-hydroxy-2'-deoxyguanosine in DNA, which is dependent on divalent cations. On the other hand, the low level of 8-OH-dG in manganese and copper deficiency might be the result of a decrease of lipid peroxidation which has been suggested to be an intermediator from active oxygen species to hydroxyl radical.
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PMID:Spontaneous and 2-nitropropane induced levels of 8-hydroxy-2'-deoxyguanosine in liver DNA of rats fed iron-deficient or manganese- and copper-deficient diets. 838 15

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

The purpose of this study was: 1) to establish the prevalence of depleted iron stores, iron deficiency, and low serum levels for copper, zinc, calcium, and magnesium in a healthy female population; and 2) to examine the effects of iron supplementation and discontinuation on the serum levels of the above minerals. One hundred eleven healthy women between the ages of 18 and 40 yr reported for fasted morning blood sampling for iron, copper, zinc, calcium, and magnesium status. Forty-five subjects were either iron-deficient as defined by a hemoglobin level below 120 g.l-1 (four subjects) or iron deplete as defined by a serum ferritin value below 20 micrograms.l-1 (43 subjects). Two subjects fit both criteria. This subgroup continued with the study and were prescribed a normal therapeutic iron dose (320 mg elemental iron per day, taken as two Slow-Fe tablets.d-1 for a period of 12 wk). The subjects then discontinued the iron supplementation for a further 12 wk. The response of the various blood minerals was monitored at 6-wk intervals. Twenty-five subjects completed the full 24-wk treatment. The main conclusions to be made from this study were that: 1) For this sample population of women, iron depletion was quite common (39%), although low hemoglobin values (< 120 g.l-1) were only seen in 3.6%. No subjects fell below the criteria for low serum copper levels (< 13.3 mumol.l-1) nor low serum magnesium levels (< 0.6 mmol.l-1). Seven subjects (6.5%) fell below the criteria for low serum zinc levels (< 11.5 mumol.l-1) while two subjects (1.8%) were below the criteria for low serum calcium levels (< 2.20 mmol.l-1). 2) Therapeutic oral iron supplementation was successful in raising mean serum ferritin values from 15.9 micrograms.l-1 to 36.5 micrograms.l-1 but was not associated with decrements in serum copper or calcium levels. 3) The treatment did not significantly effect serum zinc and magnesium levels during the supplementation period, but a downward trend continued through the discontinuation phase so that at 18 and 24 wk serum zinc and magnesium levels were significantly lower than baseline. 4) Oral contraceptive use was associated with elevated serum copper and ferritin values and lowered serum magnesium levels.
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PMID:Effects of iron supplementation and discontinuation on serum copper, zinc, calcium, and magnesium levels in women. 849 83

The presence of yeast cells in the incubation medium prevents the oxidation of ascrobate catalyzed by copper ions. Ethanol increases ascorbate retention. Pyrazole, an alcohol dehydrogenase inhibitor, prevents ascorbate stabilization by cells. Chelation of copper ions does not account for stabilization, since oxidation rates with broken or boiled cells or conditioned media are similar to control rates in the absence of cells. Protoplast integrity is needed to reach optimal values of stabilization. Chloroquine, a known inhibitor of plasma membrane redox systems, inhibits the ascorbate stabilization, the inhibition being partially reversed by coenzyme Q6. Chloroquine does not inhibit ferricyanide reduction. Growth of yeast in iron-deficient media to increase ferric ion reductase activity also increases the stabilization. In conclusion, extracellular ascorbate stabilization by yeast cells can reflect a coenzyme Q dependent transplasmalemma electron transfer which uses NADH as electron donor. Iron deficiency increases the ascorbate stabilization but the transmembrane ferricyanide reduction system can act independently of ascorbate stabilization.
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PMID:Extracellular ascorbate stabilization as a result of transplasma electron transfer in Saccharomyces cerevisiae. 874 46

This study examined the uptake of 64Cu by the brain, liver and other organs during development in rats aged 15, 21 and 63 days fed low, normal and high iron diets, using either a solution of 64CuCl2 chelated with nitrilo-triacetic acid (NTA) or 64Cu-ceruloplasmin (64Cu-Cp). 64Cu-NTA uptake was higher in the brain, spleen, kidneys, femurs and red cells at 15 days than at the later ages, while the liver took up most of the 64Cu in 63-day-old rats over the 2 h of the study. The brain had similar levels of 64Cu-NTA uptake at 15 and 21 days, even though liver uptake significantly increased, suggesting that Cu-NTA uptake by the brain increases from 15 to 21 days. The brain took up a greater percent of the injected dose of 64Cu-Cp than 64Cu-NTA yet, in either case, brain uptake was lower than that of the other organs. Iron loaded rats had significantly higher uptake of non-ceruloplasmin-bound 64Cu in all the organs examined, for at least one of the three ages, when compared with control rats. However, iron deficiency produced little change. Iron loading has a greater effect on 64Cu-Cp uptake than 64Cu-NTA, decreasing 64Cu uptake in the brain, liver, kidneys and femurs. Iron deficiency only increased 64Cu-Cp uptake in the liver. These results suggest that the mechanism of copper uptake by the liver is still maturing during suckling in the rat, and that ceruloplasmin receptor numbers are down regulated by iron loading, thus providing evidence of a new link between iron and copper metabolism.
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PMID:The effects of iron loading and iron deficiency on the tissue uptake of 64Cu during development in the rat. 878 25

Microelements deficiency is getting more and more common on account of the greatest instability in environmental balance. Normal diet does not meet all the necessities of an organism, the result of this is a great number of shortage ststes. Their manifestations are whole ranges of sufferings more or less acute. The clinical aspect of copper, zinc and iron deficiency is presented here. Correct diagnosis of microelements deficiency makes treatment procedure easier. Supplementation of appropriate amount of microelements is much more effective than traditiond, symptomatic, farmacoligical treatment.
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PMID:[Benefits and dangers connected with clinical use of microelements]. 883 59


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