beta-thalassemia/glutathione

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The relation between glutathione S-Transferase M1 null-genotype and cardiac problems in beta-thalassemia.

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This work was carried out to investigate the role of Glutathione S-Transferase M1 (GSTM1) null genotype frequency in prognosis of β-thalassemia, and to detect the correlation between GSTM1 null genotype and appearance of cardiac complications in β-thalassemia. METHODS The studied groups in the

Protection against oxidative stress in beta thalassemia/hemoglobin E erythrocytes by inhibitors of glutathione efflux transporters.

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In beta thalassemia/hemoglobin E (Hb E), abnormally high levels of oxidative stress account for accelerated senescence and increased destruction of erythrocytes. The present study aimed to investigate the role of glutathione efflux transporters, namely cystic fibrosis transmembrane conductance

Glutathione S-transferase M1 gene polymorphisms are associated with cardiac iron deposition in patients with beta-thalassemia major.

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Patients with beta-thalassemia (thal) major are subject to peroxidative tissue injury by iron overload. Glutathione S-transferases work as antioxidants, and their activity is determined genetically. In this study, we used multiplex polymerase chain reaction (m-PCR) to analyze polymorphisms of two

Glutathione S-transferase gene deletions and their effect on iron status in HbE/beta thalassemia patients.

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Iron overload and oxidative stress are main pathophysiological features of HbE/beta thalassemia patients. Glutathione S-transferase genes (GSTT1 and GSTM1) are well known detoxification agents, and any mutation in the gene is known to cause oxidative damage. This study was aimed to compare the

Glutathione redox system in β -thalassemia/Hb E patients.

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β -thalassemia/Hb E is known to cause oxidative stress induced by iron overload. The glutathione system is the major endogenous antioxidant that protects animal cells from oxidative damage. This study aimed to determine the effect of disease state and splenectomy on redox status expressed by whole

Evaluation of Glutathione-S-Transferase P1 Polymorphism and its Relation to Bone Mineral Density in Egyptian Children and Adolescents with Beta-Thalassemia Major.

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BACKGROUND Osteoporosis is a major complication of beta thalassemia major (TM). Increased oxidative stress and its controlling genes were linked to osteoporosis. Ile105 Val variant is a functional polymorphism of Glutathione S-transferase P1 (GSTP1), with reduced anti-oxidative property. No data are

Effects of silymarin on the proliferation and glutathione levels of peripheral blood mononuclear cells from beta-thalassemia major patients.

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Iron toxicity in beta-thalassemia major is the main cause of oxidative stress and cell mediated immune deficiencies. Despite indicative signs of severe oxidative deficiencies associated with beta-thalassemia major, such as decreased level of plasma antioxidants and depletion of erythrocyte

Selenium and glutathione peroxidase with beta-thalassemia major.

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BACKGROUND Chronic iron-overload is a major cause of organ failure and mortality worldwide, but its pathogenesis remains to be elucidated. OBJECTIVE To examine the relationship between various measures of body iron burden, selenium concentrations and glutathione peroxidase (GPx) activity in patients

Glutathione S-transferase gene polymorphism: Relation to cardiac iron overload in Egyptian patients with Beta Thalassemia Major.

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OBJECTIVE Estimating the prevalence of glutathione S-transferase gene polymorphism (GSTM1) null genotype among patients with beta thalassemia major (β-TM) in relation to myocardial status assessed by tissue Doppler and cardiac siderosis assessed by cardiac magnetic resonance imaging (MRI)

Glutathione S-transferase activity influences busulfan pharmacokinetics in patients with beta thalassemia major undergoing bone marrow transplantation.

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Busulfan, at a dose of 16 mg/kg, is widely used in combination with cyclophosphamide as a conditioning regimen for patients undergoing bone marrow transplantation. Wide interindividual variation in busulfan kinetics and rapid clearance of the drug have been reported, especially in children. Some of

Endothelial dysfunction and oxidant status in pediatric patients with hemoglobin E-beta thalassemia.

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Thalassemia major is characterized by anemia, iron overload, and oxidant damage to major organs, especially the cardiovascular system. Oxidative stress is ultimately involved in endothelial dysfunction, a condition which is evident in adults suffering from various cardiovascular diseases including

Plasma iron and erythrocytic glutathione peroxidase activity. A possible mechanism for oxidative haemolysis in iron deficiency anemia.

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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

Increased glutathione peroxidase activity in alpha-thalassemia.

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Glutathione peroxidase (GSHPx) activity was found to be greatly elevated in members of a family with alpha-thalassemia. Eleven other families with proven alpha-thalassemia were investigated, and all but one subject with hemoglobin H disease had increased red cell GSHPx. Most persons with

Erythropoiesis: Comparison of Cytotoxic Aldehyde Generation in Beta-Thalassemia Patients Chelated with Deferoxamine or Deferiprone (L1) Versus NO Chelation.

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The mechanism of iron-induced organ failure in iron overload disorders is not known, but it is conjectured that excess iron-catalyzed free radical generation contributes to organ damage. We hypothesized that free radical generation, quantified by the presence of 20 separate cytotoxic aldehydes in

Can hydroxyurea serve as a free radical scavenger and reduce iron overload in β-thalassemia patients?

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In this study, we hypothesize that hydroxyurea could provide an additional benefit as a free radical scavenger and/or iron chelator in β-thalassemia patients with iron overload. Twenty-one β-thalassemia intermedia patients who presented between 3 and 17 years but later required regular blood

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