Abstract
Objective: Anti-apoptotic proteins such as Bcl-2 and Bcl-xL may play a role in the survival of erythroid progenitor cells. Information about these proteins in patients with β-thalassemia minor is limited. We aimed to determine the levels of serum Bcl-2 in patients with β-thalassemia minor.Materials and Methods: Ninety-seven patients (60 females and 37 males with mean age of 29±21 years) with β-thalassemia minor were enrolled in this study. The diagnosis of β-thalassemia minor was based on whole blood counts, family history, and HbA2 levels estimated by high-performance liquid chromatography. The control group comprised 23 healthy adults (17 females and 6 males with mean age of 58±9 years) without anemia. The levels of serum Bcl-2 were measured by enzyme-linked immunosorbent assay. Mann-Whitney U tests were used in statistical evaluation and p<0.05 was accepted as statistically significant. Results: Although there was no statistically significant difference between patients with β-thalassemia minor and the control group for the level of serum Bcl-2 (p>0.05), these levels were higher in β-thalassemia minor patients than controls. Conclusion: There are damaged beta chains in β-thalassemia minor. Therefore, it is expected that premature death of red blood cells may occur due to apoptosis. The mean age of the control group was higher than that of the β-thalassemia minor group; this may be why Bcl-2 levels were higher in the β-thalassemia minor group. It is known that older age constitutes a risk for increased apoptosis. Other proteins (Bad, Bax, etc.) and pathways [CD95 (Fas) ligand] associated with apoptosis should be evaluated in future studies including more patients.
Highlights
Translations or mutations of mRNA lead to a deficiency of globin synthesis and cause thalassemia syndromes [1]
It is expected that premature death of red blood cells may occur due to apoptosis
The mean age of the control group was higher than that of the β-thalassemia minor group; this may be why Bcl-2 levels were higher in the β-thalassemia minor group
Summary
Translations or mutations of mRNA lead to a deficiency of globin synthesis and cause thalassemia syndromes [1]. Thalassemia syndromes are inherited disorders that occur as a result of abnormal synthesis of α/β-globin. Cytoplasmic inclusion bodies (including unpaired globin molecules) damage red blood cells. The life span of erythrocytes is shortened [1,2]. Cell death is regulated by many intra- and extracellular signals. The ratio of anti-apoptotic molecules (Bcl-xl, Mcl-1, Bcl-w, A1, etc.) to apoptotic molecules (Bax, Bak, Bik, Bid, etc.) determines the future of the cell [3]. The Bcl-2 protooncogene is located on chromosome 18 and inhibits the apoptotic pathway. Bcl-2 is an important molecule in the early period of cell transformation [3,4]
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Schedule a callMore From: Turkish journal of haematology : official journal of Turkish Society of Haematology
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