Journal
HEMOGLOBIN
Volume 30, Issue 2, Pages 251-256Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/03630260600642575
Keywords
glutathione S-transferase M1 (GSTM1); glutathione S-transferase T1 (GSTT1); polymorphism(s); beta-thalassemia (thal) 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 polymorphism's 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 (LVET). 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.
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