**5. Conclusions**

These findings might be related to the intra-erythrocytic chemical alterations seen in thalassemic individuals. When there is a quantitative deficiency in the alpha or beta chains, membrane-bound iron becomes free and can react with reduced glutathione, as we have shown. Perhaps, this may be one of the reasons, thalassemic cells further damage and hemolysis, leading to severe anemia in thalassemia [12]. However, iron chelators, such as deferoxamine (DFO) or deferiprone (L1), inhibited the GSH/Fe3+ mediated hemoglobin oxidation damage.

### **Acknowledgements**

This study was supported by "Qatar University internal grant QUUG-CAS-DHS- 15\16-21." The author acknowledges the support of students Anjud Khamis Al-Mohannadi, Israa Mahmoud Moursi, and laboratory technician Jaufar Pakari.
