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Query: UMLS:C0162316 (iron deficiency anemia)
 3,806 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

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

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

Autoxidation of globin chains and iron overload are the suggested mechanisms for the increased oxidative stress in beta-thalassemia. The aim of this study was to evaluate the extend of lipid peroxidation and antioxidant status of patients with beta-thalassemia and iron deficiency anemia (IDA) and compare the results with healthy subjects. Oxidant and antioxidant status of the children with beta-thalassemia major (n = 22) and iron deficiency anemia (n = 19) were studied. Healthy controls (n = 14) were age and sex matched. Fresh anticoagulated venous blood samples were obtained from all children. Conjugated diene (CD) and thiobarbituric acid-reactive (TBARS) substances were analyzed to indicate the oxidative parameters, whereas the erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GPx) were measured to show the antioxidant status of the children. Plasma TBARS and CD concentrations were elevated in beta-thalassemia compared to IDA. When compared to the controls, elevation in TBARS was significant. In the iron-deficiency group both TBARS and CD levels were decreased compared to the controls. SOD and GPx activities were increased in the beta-thalassemia group. SOD in beta-thalassemia was higher than both IDA and the controls and GPx activity was higher than the IDA group. In vivo lipid peroxidation was increased in children with beta-thalassemia major. This leads to a compensatory increase in antioxidant enzymes, whereas IDA does not lead to lipid peroxidation with a normal antioxidant enzyme activity.
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PMID:Lipid peroxidation and antioxidant status in beta-thalassemia. 1112 1

Inflammatory bowel disease is often associated with iron deficiency anemia and oral iron supplementation may be required. However, iron may increase oxidative stress through the Fenton reaction and thus exacerbate the disease. This study was designed to determine in rats with dextran sulfate sodium (DSS)-induced colitis whether oral iron supplementation increases intestinal inflammation and oxidative stress and whether the addition of an antioxidant, vitamin E, would reduce this detrimental effect. Four groups of rats that consumed 50 g/L DSS in drinking water were studied for 7 d and were fed: a control, nonpurified diet (iron, 270 mg, and dl-alpha-tocopherol acetate, 49 mg/kg); diet + iron (iron, 3000 mg/kg); diet + vitamin E (dl-alpha-tocopherol acetate, 2000 mg/kg) and the diet + both iron and vitamin E, each at the same concentrations as above. Body weight change, rectal bleeding, histological scores, plasma and colonic lipid peroxides (LPO), plasma 8-isoprostane, colonic glutathione peroxidase (GPx) and plasma vitamin E were measured. Iron supplementation increased disease activity as demonstrated by higher histological scores and heavier rectal bleeding. This was associated with an increase in colonic and plasma LPO and plasma 8-isoprostane as well as a decrease in colonic GPx. Vitamin E supplementation decreased colonic inflammation and rectal bleeding but did not affect oxidative stress, suggesting another mechanism for reducing inflammation. In conclusion, oral iron supplementation resulted in an increase in disease activity in this model of colitis. This detrimental effect on disease activity was reduced by vitamin E. Therefore, the addition of vitamin E to oral iron supplementation may be beneficial.
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PMID:Iron supplementation increases disease activity and vitamin E ameliorates the effect in rats with dextran sulfate sodium-induced colitis. 1236 9

The major purpose of this study was to compare the oxidant-related toxicities of the different oral iron preparations in children with iron deficiency anemia (IDA); the second aim was to investigate the side effects of iron preparations. Seventy-two children with IDA were randomly included in the Fe(2+) group (n = 39) or the Fe(3+) group (n = 33). Some oxidizable substrates (erythrocytes malondialdehyde (MDA), urine 8-isoprostane, and basal and Cu-stimulated-oxidized LDL and antioxidant enzyme (superoxide dismutase (SOD), catalase and glutathione peroxidase) activities were evaluated at the beginning and at the 1st, 3rd, and 6th months of therapy. Side effects due to medication were recorded. While at the end of the 1st month SOD levels were significantly increased in Fe(3+) group, at the 6th month evaluation, basal-oxidized LDL levels were significantly increased in the Fe(3+) group, as was urine 8-isoprostane in the Fe(2+) group. No other difference was found between two groups. In conclusion, there were minimal differences between children treated with ferric or ferrous iron in antioxidant system activities, the status of oxidizable substrates, and clinical toxicities.
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PMID:Safety profiles of Fe2+ and Fe3+ oral preparations in the treatment of iron deficiency anemia in children. 1616 57

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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