thalassemia/glutathione

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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

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

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

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)

Influence of glutathione S-transferase gene polymorphisms on busulfan pharmacokinetics and outcome of hematopoietic stem-cell transplantation in thalassemia pediatric patients.

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Hematopoietic stem-cell transplantation (HSCT) is currently the only curative therapeutic option for the treatment of thalassemia. In spite of the high cure rate, HSCT can lead to life-threatening adverse events in some patients. Busulfan (Bu) is a key component of the conditioning regimen prior to

Vitamin E status, glutathione peroxidase activity and the effect of vitamin E supplementation in children with thalassemia.

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Vitamin E and selenium statuses were studied in thalassemic children in comparison with 16 normal controls. Twelve Hb H disease, 46 beta-thal/Hb E and 7 beta-thal major patients had lower plasma vitamin E level than controls but plasma vitamin E/total lipids ratio of Hb H disease subjects was not

[Frequency of rheumatic heart disease, glutathione instability and thalassemia in children of Kurdish Jews].

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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

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