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

Studies were performed to determine the effects of iron deficiency on brain metabolism in rats. Concentrations of cytochrome pigments, oxidative phosphorylation, and catalase and monoamine oxidase activities in brain tissue were unaffected by iron deficiency. However, activities of aldehyde oxidase, a key enzyme in the pathway of serotonin degradation, were significantly reduced, and concentrations of serotonin and total 5-hydroxyindole compounds were elevated in brain tissue of iron-deficient animals. Aldehyde oxidase activities and concentrations of 5-hydroxyindole compounds in brain tissues returned to approximately normal values one week after treatment of iron deficient animals with iron dextran.
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PMID:Iron deficiency in the rat: biochemical studies of brain metabolism. 64 92

Whether iron deficient RBC in humans have a reduced, or an increased, susceptibility to lipid peroxidation was studied in the iron deficiency states of primary proliferative polycythaemia and iron deficiency anaemia and related to changes in the activities of iron-dependent and non-iron dependent antioxidant enzymes. Susceptibility of RBCs to lipid peroxidation was increased when expressed per g Hb. However, this was a result of the low RBC Hb giving an increased membrane lipid: Hb ratio in the incubations. Results were normal when expressed either per cell, or per ml, RBC. Glutathione reductase was normal. Increased RBC superoxide dismutase activity in iron deficiency may be explained by the younger RBC population and reductions in glutathione peroxidase and catalase activities by the microcytic hypochromic changes and the lack of availability of iron, respectively. There is no evidence of an increased susceptibility of RBC to lipid peroxidation in iron deficiency.
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PMID:Red cell lipid peroxidation and antioxidant enzymes in iron deficiency. 195 88

The content of free cholesterol, sulfhydryl groups, histidine, lipoproteins, as well as saponin resistance and catalase activity were studied in red blood cells of peripheral blood in patients with latent iron deficiency and in those with iron deficiency anemia. Significant functional disorders were detected in the red blood cells. A relationship was recorded between the changes in the red blood cell metabolism and the pattern and severity of iron deficiency.
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PMID:[Characteristics of erythrocyte metabolism in iron deficiency of varying degrees of severity]. 279 12

We developed a clear-cut nutritional iron deficiency anemia without concomittant malnutrition in rats given a low iron diet, and we restored normal iron and hemoglobin levels in these same animals with iron dextran injections. The neutrophil function studies performed during and after a period of iron deficiency showed the following: Phagocytosis of Staphylococcus aureus 502A, Streptococcus pneumoniae, and Salmonella typhimurium was not altered by iron deficiency or by the administration of iron; phagocytosis of Candida albicans was moderately abnormal during iron deficiency, and became normal with the restoration of iron sufficiency. Microbicidal activity towards Staphylococcus aureus 502A and Candida albicans, two catalase-positive microorganisms, was markedly decreased (to 50% of control values) and returned to normal when iron sufficiency was restored. Killing of a catalase-negative organism, Streptococcus pneumoniae was normal in iron-deficient rats. This pattern of differential bactericidal activities suggested an abnormality of the oxidant radical-generating machinery in neutrophils of iron-deficient animals. Indeed, iron deficiency caused a marked decrease of neutrophil nitroblue tetrazolium dye reduction, which disappeared after iron administration. Neutrophil myeloperoxidase activity was slightly decreased in iron deficient rats and returned to normal after iron administration. Microbicidal activity towards a gram-negative, catalase-positive organism, Salmonella typhimurium, was equal in iron deficient and iron sufficient animals. Our combined results suggest that a definite microbicidal defect is the consequence of nutritional iron deficiency, apart from any protein-calorie malnutrition. This defect affects the disposal in PMNs of two catalase-positive microorganisms (which require intracellular production of oxidant radicals for their destruction) but not of a catalase-negative bacterial species.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neutrophil bactericidal dysfunction towards oxidant radical-sensitive microorganisms during experimental iron deficiency. 608 85

The response of glutathione peroxidase (GSH-Px) to dietary iron deficiency was studied in red blood cells and liver from male Sprague-Dawley rats. A casein-based purified diet containing 0.02 ppm Se and 7 ppm Fe was used as the basal diet. Rats were given the basal diet supplemented with either 0.5 ppm Se or 30 ppm Fe or both for 10 weeks. Food consumption in iron-deficient rats was 79% of controls. Iron deficiency caused a significant decrease of GSH-Px and catalase activities in red blood cells (RBC) expressed per cell. However, enzyme activities expressed per gram of hemoglobin or per milligram or protein increased. These data suggest that GSH-Px is present in adequate quantities in iron-deficient red blood cells to protect cell membranes and hemoglobin as long as the rats receive adequate Se. Hepatic catalase was not altered by iron or Se deficiency. Liver Se GSH-Px activity/g tissue decreased to 75% of control activity during iron deficiency. Non Se GSH-Px activity increased during Se or iron deficiencies and may compensate to a limited extent for decreased Se GSH-Px activity. In contrast to earlier reports, RBC GSH-Px activity was not altered by iron deficiency except for possible indirect effects related to changes in red blood cell size or food intake.
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PMID:Glutathione peroxidase activity in iron-deficient rats. 745 71

A comparative study has been made on the mechanisms of toxicities of trivalent and hexavalent forms of chromium in Neurospora crassa. Of the two forms, Cr6+ is more toxic than Cr3+. The toxicity of Cr3+ was found to be due to its specific antagonism with iron uptake. Fe3+ was found to be very effective in reversing the toxicity of Cr3+ by concomitantly suppressing its uptake. That the Cr3+ toxicity caused a conditional intracellular iron deficiency was indicated by the decrease in the activities of catalase and uricase and a progressive increase in the excretion of iron binding compound into the medium. The toxicity of Cr6+ (as Cr2O7(2-)) was found to be due to its specific antagonism of sulfate uptake. Methionine was found to be more effective in reversing dichromate toxicity than sulfate, probably by repressing the synthesis of sulfate permeases responsible for dichromate (Cr6+) uptake. Maximal uptake of Cr6+ was nearly tenfold lower and Vmax much higher than that of Cr3+. Evidence has been adduced to show that Cr6+ and Cr3+ were toxic by themselves and that interconversion between the tri- and hexavalent forms of chromium did not occur to any detectable extent.
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PMID:Chromium toxicity in Neurospora crassa. 779 96

The studies of lipid peroxidation, antioxidant defence, structure and functions of erythrocytes in iron deficiency of painters revealed severe changes in the cells' chemiluminescence, sulfhydryl and catalase activities, levels of free cholesterol, lipoproteins, hystidine and glucose-6-phosphate dehydrogenase, saponin resistance and viscosity of erythrocytes. The changes appeared to depend on duration of exposure to the toxic chemicals. The data presents additional markers of toxic influence on erythrocytes in developing iron deficiency of painters.
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PMID:[Erythrocyte structure and function in iron-deficiency states in painters]. 783 28

Many genes whose transcription is erythroid-specific contain enhancer or promoter elements that bind the transcription factor NF-E2. Hemin induction increases the expression of globin genes in the human erythroleukemia cell line K562, and increases the expression of reporters gene regulated by an enhancer elements containing binding sites for NF-E2. The failure of metalloporphyrins other than hemin to stimulate the transient expression of a CAT reporter gene linked to an enhancer element containing a binding site for NF-E2 was correlated with their failure to induce benzidine-positive K562 cells and increase the steady-state level of gamma-globin mRNA. This study suggests that elevated levels of zinc protoporphyrin IX found in the anemia of chronic disease, iron deficiency, and lead poisoning may contribute to a decrease in globin gene expression by interfering with the transcriptional activity of enhancer elements containing binding sites for NF-E2.
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PMID:Iron protoporphyrin IX (hemin) but not tin or zinc protoporphyrin IX can stimulate gene expression in K562 cells from enhancer elements containing binding sites for NF-E2. 804 43

Chronic exposure of adult rats to dietary intake of cadmium (15 mg CdCl2/day/kg for 30 days) leads to development of anemia and thrombocytosis. Anemia is characterized by significant reticulocytosis (13.1 +/- 1.0%), anysocytosis, poikilocytosis, iron deficiency and marked alterations of antioxidant and metabolic status of red blood cells. Activities of SOD, catalase, GPx and GR were significantly increased in red blood cells of cadmium-treated rats. In treated animals cadmium induced an increase of red cell reduced and oxidized glutathione with no changes of GSSG/GSH ratio. However, significant reduction of lipid peroxidation was found. Plasma levels of tocopherol and ascorbate, as well as activity of glutathione-S-transferase, were all significantly increased in cadmium-treated rats. The energy metabolism of red blood cells was deeply altered in cadmium-treated rats. The levels of ATP, ADP, AMP and TAN were significantly increased while ATP/ADP ratio and adenylate energy charge (AEC) were significantly reduced. The level of 2,3-BPG was somewhat lower, but 2,3-BPG/Hb ratio was considerably higher, in red blood cells of cadmium-treated rats.
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PMID:Cadmium-induced changes of antioxidant and metabolic status in red blood cells of rats: in vivo effects. 837 Apr 23

Iron deficiency has been implicated in increasing the risk of GI tract cancers in humans. Among various mechanisms of carcinogenesis, oxidative damage to DNA is well known and, hence, the present experimental study was undertaken to investigate lipid peroxidation and activities of different antioxidant enzymes in iron deficiency to explain the higher risk of tumorigenesis. Two groups of male weanling Fischer rats maintained on iron sufficient (C) or iron deficient (D) diets for a period of 32 weeks were subdivided, from 3 weeks onwards, into two subgroups each. The carcinogen, dimethyl hydrazine was fed at a dose of 30 mg/kg/week IG for a period of 9 weeks to groups that were designated as (C+) and (D+). The other two subgroups (C-) and (D-) served as controls. After the experimental period, hepatic assays for lipid peroxidation (MDA production) and activities of various antioxidant enzymes were carried out. The results showed that MDA production was elevated by 50% and activity of superoxide dismutase significantly depressed in carcinogen-fed, iron-deficient group (D+) by 28% compared to deficient (D-) group. There was an increase in hepatic selenium-dependent glutathione peroxidase activity in iron-deficient and iron-deficient, carcinogen-treated groups to the extent of 57 and 59%, respectively, as compared to controls; however, induction of enzyme in response to carcinogen feeding, observed in the control group, was not evident in iron deficiency. Liver catalase was not altered between control and deficient groups. These results suggest that prolonged iron deficiency superimposed with carcinogen ingestion may render the host susceptible to a greater risk of tumorigenesis through oxidative stress.
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PMID:Lipid peroxidation and activities of antioxidant enzymes in iron deficiency and effect of carcinogen feeding. 879 Oct 98


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