Association of ghost Na+/K+-ATPase activity and 2,3-bisphosphoglycerate levels with deferoxamine use in β-thalassemia

  • N. A. Al-Jabouri University of Babylon
  • E. H. Al-Rikabi University of Babylon
  • O. M. Y. Al-Zamely University of Babylon
Keywords: β-thalassemia, Na /K -ATPase, 2,3-bisphosphoglycerate.

Abstract

β - t halassemia is set of genetic illnesses defined by abnormalities in the synthesis of the beta chains of hemoglobin . A broad spectrum of phenotypes is observed, they are presented inside red blood cells . 2,3-bisphosphoglycerate (2,3-bpg) is a key comp o nent that controls the hemoglobin's oxygen binding. The study examined the effect of the drug deferoxamine on the levels of 2,3-bisphosphoglycerate, Na + /K + ATPase in patients with thalassemia type beta. The study was a case-control study. A total of 130 individuals were involved: a total of 70 patients with β -thalassemia, 60 healthy controls. The initial group was carefully selected based on the patients' clinical symptoms. The 2,3-bisphosphoglycerate level was determined by using the enzyme -linked imm u ne sorbent assay (ELISA ) , while Na + /K + ATPase was measured by ghost . Patients e xhibited elevated 2,3-bisphosphoglyce rate levels in comparison to the control group, accompanied by elevated Na + /K + ATPase levels in patients compar ed to the controls. Elevated levels of 2,3- b isphosphoglycerate dehydrogenase in β- thalassemia patients are due to increased hemolysis, as it is formed within the red blood cell as a result of glycolysis. The level of s odium potassium ATPase, present in the red blood cell membrane, also rises during red blood cell breakdown.

References

Ansharullah, B. A., Sutanto, H., & Romadhon, P. Z. (2025). Thalassemia and iron overload cardiomyopathy: Pathophysiological insights, clinical implications, and management strategies. Current Problems in Cardiology, 50(1), 102911.

Bunn, H. F. (2022). Oxygen delivery in the treatment of anemia. New England Journal of Medicine, 387(25), 2362–2365.

Cappellini, M. D. (2012). The thalassemias. In: Goldman, L., & Schafer, A. I. (Eds.). Goldman’s Cecil Medicine. Twenty-fourth edition. Vol. 1. Elsevier Saunders. Pp. 1060–1066.

Fibach, E., & Rachmilewitz, E. A. (2017). Pathophysiology and treatment of patients with beta-thalassemia – an update. F1000Research, 6, 2156.

Galanello, R., & Cao, A. (2011). Alpha-thalassemia. Genetics in Medicine, 13(2), 83–88.

Geering, K. (2008). Functional roles of Na,K-ATPase subunits. Current Opinion in Nephrology and Hypertension, 17(5), 526–532.

Haidas, S., Zannos-Mariolea, L., & Matsaniotis, N. (1975). Red cell 2,3‐diphosphoglycerate levels in children with hereditary haemolytic anaemias. British Journal of Haematology, 31(4), 521–530.

Hirsch, R. E., Sibmooh, N., Fucharoen, S., & Friedman, J. M. (2017). HbE/β-thalassemia and oxidative stress: The key to pathophysiological mechanisms and novel therapeutics. Antioxidants and Redox Signaling, 26(14), 794–813.

Jorge, S. E., Ribeiro, D. M., Santos, M. N. N., & de Fátima Sonati, M. (2016). Hemoglobin: Structure, synthesis and oxygen transport. In: Costa, F. F., & Conran, N. (Eds.). Sickle cell anemia. From basic science to clinical practice. Springer, Cham. Pp. 1–22.

Lyu, J., Ni, M., Weiss, M. J., & Xu, J. (2024). Metabolic regulation of erythrocyte development and disorders. Experimental Hematology, 131, 104153.

Muncie Jr., H. L., & Campbell, J. (2009). Alpha and beta thalassemia. American Family Physician, 80(4), 339–344.

National Center for Biotechnology Information (2025). PubChem Compound Summary for CID 9548671, 2,3-bisphosphoglycerate.

Omar, A. K., Ahmed, K. A., Helmi, N. M., Abdullah, K. T., Qarii, M. H., Hasan, H. E., Ashwag, A., Nabil, A. M., Abdu, A.-G. M., & Salama, M. S. (2017). The sensitivity of Na+/K+-ATPase as an indicator of blood diseases. African Health Sciences, 17(1), 262–269.

Patel, S., Jose, A., & Mohiuddin, S. S. (2023). Physiology, oxygen transport and carbon dioxide dissociation curve. StatPearls Publishing, Treasure Island.

Pivovarov, A. S., Calahorro, F., & Walker, R. J. (2018). Na+/K+-pump and neurotransmitter membrane receptors. Invertebrate Neuroscience, 19(1), 1.

Sadiq, I. Z., Abubakar, F. S., Usman, H. S., Abdullahi, A. D., Ibrahim, B., Kastayal, B. S., Ibrahim, M., & Hassan, H. A. (2024). Thalassemia: Pathophysiology, diagnosis, and advances in treatment. Thalassemia Reports, 14(4), 81–102.

Salamone, F. A. (1999). Drake, St. Clair, Jr. (02 January 1911–15 June 1990), anthropologist. American National Biography Online.

Shafique, F., Ali, S., Almansouri, T., Van Eeden, F., Shafi, N., Khalid, M., Khawaja, S., Andleeb, S., & Hassan, M. U. (2021). Thalassemia, a human blood disorder. Brazilian Journal of Biology, 83, e246062.

Sun, K., Liu, H., Song, A., Manalo, J. M., D’Alessandro, A., Hansen, K. C., Kellems, R. E., Eltzschig, H. K., Blackburn, M. R., Roach, R. C., & Xia, Y. (2017). Erythrocyte purinergic signaling components underlie hypoxia adaptation. Journal of Applied Physiology, 123(4), 951–956.

Taher, A. T., & Saliba, A. N. (2017). Iron overload in thalassemia: Different organs at different rates. Hematology, 2017(1), 265–271.

Webb, K. L., Dominelli, P. B., Baker, S. E., Klassen, S. A., Joyner, M. J., Senefeld, J. W., & Wiggins, C. C. (2022). Influence of high hemoglobin-oxygen affinity on humans during hypoxia. Frontiers in Physiology, 12, 763933.

Zhang, X., Lee, W., & Bian, J.-S. (2022). Recent advances in the study of Na+/K+-ATPase in neurodegenerative diseases. Cells, 11(24), 4075.

Zhou, G., Dada, L. A., & Sznajder, J. I. (2008). Regulation of Na,K-ATPase by reactive oxygen species. Current Topics in Membranes, 61, 131–146.

Published
2025-11-08
How to Cite
Al-Jabouri, N. A., Al-Rikabi, E. H., & Al-Zamely, O. M. Y. (2025). Association of ghost Na+/K+-ATPase activity and 2,3-bisphosphoglycerate levels with deferoxamine use in β-thalassemia. Regulatory Mechanisms in Biosystems, 16(4), e25212. https://doi.org/10.15421/0225212