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Glutathione S-transferase M1 gene polymorphisms are associated with cardiac iron deposition in patients with beta-thalassemia major.
- Source :
-
Hemoglobin [Hemoglobin] 2006; Vol. 30 (2), pp. 251-6. - Publication Year :
- 2006
-
Abstract
- 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 endogenous antioxidant agents, glutathione S-transferase M1 (GSTM1) and glutathione S-transferase T1 (GSTT1), and to determine their roles in 41 patients with beta-thal major. Our results showed that the GSTM1 and GSTT1 null genotypes were not associated with any incidence of endocrine dysfunction (including diabetes mellitus, hypogonadism, hypothyroidism, and growth hormone deficiency), liver function, or impaired left ventricular ejection fraction (LVEF). The GSTM1 null genotype, but not the GSTT1 null genotype, was associated with a decreased signal intensity ratio on cardiac magnetic resonance imaging (MRI). Our results suggest that genetic variations of the GSTM1 enzyme are associated with cardiac iron deposition in patients with beta-thal major.
- Subjects :
- Adolescent
Adult
Cardiomyopathies enzymology
Cardiomyopathies etiology
Chelation Therapy
Child
Combined Modality Therapy
Comorbidity
Deferiprone
Deferoxamine therapeutic use
Female
Genetic Predisposition to Disease
Genotype
Humans
Iron metabolism
Iron Chelating Agents therapeutic use
Iron Overload etiology
Iron Overload genetics
Male
Oxidative Stress
Polymorphism, Genetic
Pyridones therapeutic use
Stroke Volume
Transfusion Reaction
beta-Thalassemia drug therapy
beta-Thalassemia enzymology
beta-Thalassemia therapy
Cardiomyopathies genetics
Glutathione Transferase genetics
Iron Overload enzymology
beta-Thalassemia complications
Subjects
Details
- Language :
- English
- ISSN :
- 0363-0269
- Volume :
- 30
- Issue :
- 2
- Database :
- MEDLINE
- Journal :
- Hemoglobin
- Publication Type :
- Academic Journal
- Accession number :
- 16798650
- Full Text :
- https://doi.org/10.1080/03630260600642575