Attenuation of xanthine oxidase activity: A hypothesis for limiting reactive oxygen species-induced vascular damage in patients with β-thalassemia
Issued Date
2025-07-01
Resource Type
ISSN
03069877
eISSN
15322777
Scopus ID
2-s2.0-105007469229
Journal Title
Medical Hypotheses
Volume
200
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SCOPUS
Bibliographic Citation
Medical Hypotheses Vol.200 (2025)
Suggested Citation
Noulsri E., Lerdwana S. Attenuation of xanthine oxidase activity: A hypothesis for limiting reactive oxygen species-induced vascular damage in patients with β-thalassemia. Medical Hypotheses Vol.200 (2025). doi:10.1016/j.mehy.2025.111686 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/110689
Title
Attenuation of xanthine oxidase activity: A hypothesis for limiting reactive oxygen species-induced vascular damage in patients with β-thalassemia
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Abstract
Vascular damage in individuals with β-thalassemia is a significant complication that increases the risk for thrombosis and cardiovascular disorders. An increasing body of research indicates that iron accumulation and elevated reactive oxygen species (ROS) levels play critical roles in the vascular pathology associated with β-thalassemia. Current therapeutic strategies are predominantly confined to the administration of various antioxidants, highlighting the urgent need for innovative, targeted treatments that specifically address vascular complications. Xanthine oxidase (XO) is a crucial enzyme in the purine metabolic pathway, where the degradation of purine nucleotides results in the production of ROS. Therefore, we suggest that increased XO activity contributes to vascular damage in β-thalassemia by inducing ROS production. Our suggestion is supported by existing literature, which demonstrates: 1) an association between increased XO activity and ROS-induced vascular damage; 2) the presence of hypoxia, an inflammatory state, heightened destruction of erythroblasts in the bone marrow, and increased heme metabolism in the liver of patients, all of which may stimulate XO activity and expression; and 3) the potential for reducing XO activity through the application of inhibitors, which may provide therapeutic opportunities for the treatment of β-thalassemia. Although several aspects warrant further investigation, our proposed strategy of combining XO inhibition with existing antioxidant therapies may represent a promising approach to mitigate the detrimental effects of ROS-induced vascular damage in patients with β-thalassemia patients.