Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162316 (iron deficiency anemia)
 3,806 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The red cell glutathione-peroxidase (GSH-Px) activity of 9 normal subjects is compared with that of 15 cases of iron deficiency anaemia and with 13 cases of heterozygous beta-thalassemia with the same degree of anaemia and hypochromia. 2 cases of sideroblastic anaemia with high serum iron levels were also examined. Enzymatic activity was found to be significantly decreased in iron deficiency anaemia (about 55% of normal range), while it was not affected in heterozygous beta thalassaemia and it was increased in the 2 cases of sideroblastic anaemia. Moreover, GSH-Px activity exhibited a significant correlation with serum iron levels in all the patients studied. The observed modifications in GSH-Px activity are not correlated with erythrocyte ageing because reticulocyte-poor fractions exhibited GSH-Px activity which was not significantly reduced in respect of the reticulocyte-rich ones. These data seem to suggest that iron has a crucial connection with erythrocyte GSH-Px and that the enzyme deficiency may be of some importance in explaining the decreased red cell survival observed in severe iron-deficiency anaemias.
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PMID:Plasma iron and erythrocytic glutathione peroxidase activity. A possible mechanism for oxidative haemolysis in iron deficiency anemia. 96 43

Neutrophil glutathione peroxidase (GSH-Px) activity was studied in 30 children with nutritional iron deficiency anaemia and 25 healthy age-matched controls. Initially GSH-Px in iron deficient anaemic children was significantly (p less than 0.001) low compared to the control group. All patients were subjected to iron therapy but only 8 returned for follow-up. The GSH-Px activity in all 8 cases rose to normal levels after therapy. These results suggest a relationship between iron and GSH-Px activity.
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PMID:Neutrophil glutathione peroxidase activity in iron deficiency anaemia. 395 65

The activity of 18 red blood cell (RBC) enzymes and reduced glutathione (GSH) content were measured in 70 normal subjects, in 50 heterozygous beta-thalassaemia carriers and in 50 non-thalassaemic patients with haemolytic anaemia and high reticulocyte counts. In addition, pyrimidine 5'nucleotidase (P5N) activity was also determined in 34 patients with hypochromic, microcytic, iron deficiency anaemia. beta-Thalassaemia trait was associated with an increase in almost all of the enzyme activities, except for 2,3-bisphosphoglycerate synthetase (BPGS) and glutathione reductase (GR) which were normal and for acetylcholinesterase (AChE) and P5N which were slightly and markedly decreased respectively. The increases in enzyme activities were similar to those observed in patients with non-thalassaemic reticulocytosis except for glyceraldehydephosphate dehydrogenase (GAPD), phosphoglyceratekinase (PGK), pyruvate kinase (PK), glutathione peroxidase (GPX) and adenylate kinase (AK) which were higher than in non-thalassaemic group of patients with increased number of reticulocytes. No correlation was found between the severity of P5N deficiency and the intensity of basophilic stippling which was present in 46 of 50 thalassaemic carriers here studied. In addition, GSH content and UV absorption spectra of deproteinized thalassaemic RBC extracts were also found to be normal. The present findings provide further information on the metabolic status of RBC in beta-thalassaemia trait and suggest a possible molecular explanation for the frequently observed basophilic stippling in this disease.
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PMID:Pyrimidine 5'nucleotidase and several other red cell enzyme activities in beta-thalassaemia trait. 632 Aug 62

Patients with iron deficiency anemia (IDA) were examined as well as patients with active lymphoma with low serum iron (SI) and anemia prior to treatment. Increased content of reduced glutathione (GSH) was found in the patients with IDA as well as enhanced activity of PBG-S in erythocytes, in parallel with the decreased SI and saturation rate of transferrins (SRT) and enhanced total iron-binding capacity (TIBC) in serum. In lymphoma patients a normal GSH content is found as well as normal PBG-S activity in erythocytes, low content of iron, SRT level and decreased TIBC in serum. The connection of SH groups with the level of serum iron is discussed.
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PMID:[Reduced glutathione and porphobilinogen synthase activity in the erythrocytes of anemic patients with low serum iron]. 714 24

Oxidative damage to erythrocytes in thalassaemia has been related to generation of free radicals by an excess of denaturated alpha- or beta-globin chains, intracellular iron overload and low concentration of normal haemoglobin (HGB). Two good indicators of such oxidative damage are the high red blood cell (RBC) malonyldialdehyde (MDA) production detected following exogenous oxidant stress and the decrease of pyrimidine 5'-nucleotidase (P5N), the most sensitive enzyme to SH-group damage in vivo. Conflicting data, however, have so far accumulated in the literature concerning differences in oxidative damage between the different forms of thalassaemia and iron deficiency anaemia (IDA). In the present study, oxidative susceptibility, as defined by the production of MDA in vitro and antioxidant capacity, as measured by the activity of RBC glutathione peroxidase (GPx), superoxide dismutase (SOD) and by reduced glutathione (GSH), have been studied in microcytic RBCs from patients with beta-thalassaemia trait, Spanish (delta beta) zero-thalassaemia heterozygotes (delta beta-thalassaemia trait) and iron deficiency anaemia (IDA). The results are consistent with the existence of significant differences in the severity and pattern of oxidative stress susceptibility between beta-thalassaemia trait (increased MDA production and higher SOD and GPx activities) and the other two forms of microcytosis (delta beta thalassaemia trait and IDA). Furthermore, the finding of normal P5' N activity in delta beta thalassaemia trait, gives further support to the less intense peroxidative environment of RBCs in this form of thalassaemia when compared to beta-thalassaemia trait, characterized by acquired RBC P5' N deficiency due to oxidative damage.
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PMID:Increased susceptibility of microcytic red blood cells to in vitro oxidative stress. 749 80

Red blood cells in iron deficiency anemia (IDA) have a decreased activity of essential antioxidant enzymes. The present study examined the effect of in vitro exposure to oxidative agents in IDA cells and their recovery capacity. Red cells of 26 IDA patients and 10 healthy subjects were examined. Cells of IDA patients had higher levels of reduced glutathione (GSH), and normal methemoglobin and malonyldialdehyde (MDA) levels. Exposure to butyl hydroperoxide revealed a dose-dependent sensitivity in IDA cells, with extensive GSH depletion and increased MDA levels. These changes were partially reversible by incubation with dithiothreitol. Exposure to phenazine methosulfate, to produce intracellular superoxide ions, resulted in moderate GSH depletion and methemoglobin production. IDA cells were more sensitive than control cells to high concentrations of this substance. This effect was further augmented by preincubation with a superoxide dismutase inhibitor. Our data demonstrate that IDA cells are more susceptible to oxidation but have good capacity for recovery.
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PMID:Iron deficiency anemia: recovery from in vitro oxidative stress. 809 40

Antioxidant defence was investigated in red blood cells (RBC) in 56 patients with 3 different haemoblastoses: polycythemia vera (PV), chronic myelogenous leukaemia (CML), chronic lymphoid leukemia (CLL) with and without anaemia, in 12 iron deficiency anaemia (A) patients and 50 healthy persons. The activities were determined of the following antioxidant enzymes: glucose-6-phosphate dehydrogenase (G6PD), glutathione reductase (GSSG-R), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalase (CAT) and MDA levels. Antioxidant defence is decreased and the level of lipid peroxidation are increased in RBC in all patients (PV, CML, CLL, A). Different changes were detected in the antioxidative defence between normal red blood cells and those formed from leukaemic cells clone. In normal RBC in anaemia (CLL, A) opposite deviation of G6PD and GSSG-R activities was observed. In RBC formed from leukaemic cell clone (PV, CML), a simultaneous significant increase in G6PD and GSSG-R activities was found, which indicated activisation of pentose phosphate pathways (PPP) in these pathologies; in anaemia they function less effectively.
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PMID:Anaemia and antioxidant defence of the red blood cells. 1021 69

Oral iron-supplementation is a general practice to correct iron deficiency anemia. Exposure of iron-deficient intestine to large doses of iron is known to induce oxidative damage, leading to loss of functional integrity, and reduced mucosal cell turnover. Conditioning of intestine with anti-oxidants during iron administration was shown to suppress iron-induced oxidative damage. Zinc is known to protect cells from peroxidative damage by inducing metallothionein and maintaining the sulfhydryl group stability. Nevertheless, co-administration of iron and zinc may antagonize each other with respect to absorption. In the present study, we show that combined supplementation of iron and zinc though marginally inhibits iron uptake significantly attenuates the oxidative stress by induction of metallothionein and elevating the levels of GSH. Further, presence of zinc in situ reduced the iron-induced hydroxyl radical production in the intestinal mucosa, as assessed by EPR spectroscopy. These results strongly suggest a protective role for zinc on iron-induced oxidative stress, which might have implications in anemia control programs.
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PMID:A protective role for zinc on intestinal peroxidative damage during oral iron repletion. 1514 71

The present study was designed to evaluate the effect of a new iron tonic (squid ink melanin-Fe [SM-Fe]) on remission of iron deficiency anemia (IDA) using a rat model of IDA. The rat IDA model was established with low-iron diet feeding and caudal vein blooding. Then different dosages of SM-Fe were given to the rats once a day by intragastric administration, with FeSO4 and FeCl3 as positive control. The content of Hemoglobin (Hb), red blood cell (RBC), hematocrit (HCT), and mean corpuscular volume (MCV) were analyzed in addition to the contents of serum iron (SI) and intracellular free erythrocyte protoporphyrin (FEP). The content of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in serum was also measured. The results showed that anemia caused by iron deficiency was established as a consequence of the low-iron diets. SM-Fe showed an effective restoration action by returning Hb, RBC, HCT, MCV, SI, and FEP in IDA animals to normal values. An antioxidant effect was also observed that reduced MDA level, enhanced the activities of SOD and GSH-Px in serum, and protected erythrocytes from the injury of reactive oxygen species as a consequence of SM-Fe intake. In comparison with FeSO4 and FeCl3, higher bioavailability of iron and fewer side effects were also observed. In conclusion, SM-Fe remitted iron deficiency anemia symptoms significantly, suggesting that SM-Fe might contribute to improving hemopoietic function in IDA rats and might be exploited as a safe, efficient new iron tonic.
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PMID:Effect of squid ink melanin-Fe on iron deficiency anemia remission. 1901 17

We propose that oxidative damage may play a role in the pathogenesis of iron deficiency anaemia (IDA). Participants were selected from Basic Attention Ambulatory from North of Rio Grande do Sul, Brazil. All subjects were older than 65 years - 17 patients with IDA and primary hypertension and 18 patients with primary hypertension (control group) were included in the present study. We measured antioxidant defenses including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and total glutathione (GSH) by spectrophotometric assays. We also determined protein oxidative damage in haemolysate and plasma by carbonyl assay. We characterized the lipid peroxidation by malondialdehyde (MDA) accumulation. The results show that IDA patients had significantly higher CAT and SOD levels than controls. GPx activity was not different between the groups. Oxidative protein damage was noted in the plasma but not in the haemolysate. A significantly enhanced production of MDA was observed in the serum of IDA patients, as an indication of increased level of auto-oxidizable lipids under oxidative stress. These results support the idea that patients with IDA are subjected to chronic oxidative stress. Therefore it is important that IDA in older persons receives adequate attention in clinical practice and is not considered simply a part of normal aging.
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PMID:Oxidative stress in older patients with iron deficiency anaemia. 1965 48


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