Assessment of Na+/K+ ATPase and Certain Metal Ions Resulting from the Impact of Deferoxamine in Beta-Thalassemia Patients
DOI:
https://doi.org/10.36320/ajb/v17.i2.20068Keywords:
Na/K Atpase, sodium, potassiumAbstract
Background: Thalassemia is a genetic disease that is autosomal in nature. The condition is marked by an impaired capacity for the synthesis of polypeptides. The presence of chains of normal hemoglobin has been observed to result in the development of anemia. This phenomenon persists as a significant health concern. The Mediterranean region is characterized by a distinct culinary tradition, with a variety of dishes influenced by the region's geographical and historical context.
Aim of Study: This study was designed to evaluate the activity of sodium potassium ATPase in the red blood cell membrane of thalassemia patients as well as some metal ions (sodium, potassium, magnesium, total iron) as a result of the effect of deferoxamine treatment.
Methods: A total of 130 individuals were involved in this case-control study:70Patients with beta thalassemia aged (1±25years ), 60 healthy controls aged (2±25yaers). The initial group was carefully selected based on the patients' clinical symptoms. Evaluation of sodium, potassium, magnesium, and iron levels was completed by spectrophotometry. Enzyme activity was expressed as micrograms of phosphate concentration per gram of total protein concentration in red blood cells.
Results: The average enzyme activity was significantly (P<0.001) higher in beta thalassemia patients (1000 ±248) µg Pi/mg protein. min compared to healthy individuals (481±160) µg Pi/mg protein. min. Also, sodium levels were significantly(P<0.001) higher in thalassemia patients compared to the control group. We also noticed that iron levels were higher compared to the control group, while noting that there was no significant(P<0.05) change in magnesium and potassium levels in patients compared to healthy individuals.
Conclusions: Elevated sodium potassium phosphate (ATPase) levels result from changes in the cell membrane and the breakdown of red blood cells, which increases sodium permeability and increases the activity of this enzyme. Elevated sodium levels are often caused by kidney disorders due to iron overload, a condition caused by repeated blood transfusions. The body lacks an effective mechanism for disposing of excess iron, leading to its accumulation in the blood and organs (iron overload). In thalassemia, the body also increases iron absorption from the intestine due to false signals from hemoglobin deficiency, which exacerbates the condition. It was also noted that there was no change in potassium and magnesium levels in thalassemia patients, due to the fact that these elements are not affected by increased iron levels except in very advanced cases of organ failure
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References
1. Haydir K. Al-Jezani1, Oda M. Al-Zamely. (2021). Red Cell Na+/K+- Atpase (NKA) Activity and Serum Electrolyte, Annals of R.S.C.B., ISSN:1583-6258, Vol. 25, Issue 6, 2021, Pages. 8166 – 8174 Received 25 April 2021; Accepted 08 May 2021 Concentration of Patients with Major Thalassemia Disease in Babylon Province/Iraq, [email protected] .
2. Contreras, R. G., Torres-Carrillo, A., Flores-Maldonado, C., Shoshani, L., & Ponce, A. (2024). Na+/K+-ATPase: More than an Electrogenic Pump. International journal of molecular sciences, 25(11), 6122
3. Al-Rikabi, Eman & Jaafar, Mazin & Yasser, Oda. (2021). Estimation of NaK - ATPase Enzyme Activity and Endogenous Digitalis in Patients with Diabetic Neuropathy. NeuroQuantology. 19. 95-103.
4. Brady S, Siegel G, Albers RW, Price D. (2012). Basic Neurochemistry: Principles of Molecular, Cellular and Medical Neurobiology, 8th edn. Massachusetts, USA: Elsevier Academic Press.; 41-62.
5. Cianciulli P. (2009). Iron chelation therapy in thalassemia syndromes. Mediterranean journal of hematology and infectious diseases, 1(1), e2009034.
6. Piskin, E., Cianciosi, D., Gulec, S., Tomas, M., & Capanoglu, E. (2022). Iron Absorption: Factors, Limitations, and Improvement Methods. ACS omega, 7(24), 20441–20456. https://doi.org/10.1021/acsomega.2c01833
7. Suhaimi, S. A., Zulkipli, I. N., Ghani, H., & Abdul-Hamid, M. R. W. (2022). Applications of next generation sequencing in the screening and diagnosis of thalassemia: A mini-review. Frontiers in pediatrics, 10, 1015769. https://doi.org/10.3389/fped.2022.1015769.
8. Ansari, S., Azarkeivan, A., Miri-Aliabad, G., Yousefian, S., & Rostami, T. (2017). Comparison of iron chelation effects of deferoxamine, deferasirox, and combination of deferoxamine and deferiprone on liver and cardiac T2* MRI in thalassemia maior. Caspian journal of internal medicine, 8(3), 159–164. https://doi.org/10.22088/cjim.8.3.1597-
9. Cappellini, M. D., Cohen, A., Porter, J., Taher, A., & Viprakasit, V. (Eds.). (2014). Guidelines for the Management of Transfusion Dependent Thalassaemia (TDT). (3rd ed.). Thalassaemia International Federation.Cohen, A., Porter, J., Taher, A., & Viprakasit, V. (Eds.). (2014). Guidelines for the Management of Transfusion Dependent Thalassaemia (TDT). (3rd ed.). Thalassaemia International Federation..
10. Kassák, P., Sikurová, L., Kvasnicka, P., & Bryszewska, M. (2006). The response of Na+/K+ -ATPase of human erythrocytes to green laser light treatment. Physiological research, 55(2), 189–194. https://doi.org/10.33549/physiolres.930711
11. Baykov, A. A., Evtushenko, O. A., & Avaeva, S. M. (1988). A malachite green procedure for orthophosphate determination and its use in alkaline phosphatase-based enzyme immunoassay. Analytical biochemistry, 171(2), 266–270. https://doi.org/10.1016/0003-2697(88)90484-8
12. 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. M., & Salama, M. S. (2017). The sensitivity of Na+, K+ ATPase as an indicator of blood diseases. African health sciences, 17(1), 262–269. https://doi.org/10.4314/ahs.v17i1.32
13. Zhang, X., Lee, W., & Bian, J. S. (2022). Recent Advances in the Study of Na+/K+-ATPase in Neurodegenerative Diseases. Cells, 11(24), 4075. https://doi.org/10.3390/cells11244075
14. 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 & redox signaling, 26(14), 794–813. https://doi.org/10.1089/ars.2016.6806
15. Sadiq IZ, Abubakar FS, Usman HS, Abdullahi AD, Ibrahim B, Kastayal BS, Ibrahim M, Hassan HA (2024). Thalassemia: Pathophysiology, Diagnosis, and Advances in Treatment. Thalassemia Reports.; 14(4):81-102.
16. Bajwa H, Basit H. Thalassemia. [Updated 2023 Aug 8]. In: StatPearls
17. Zhang H, Zhabyeyev P, Wang S, Oudit GY. (2019). Role of iron metabolism in heart failure: From iron deficiency to iron overload. Biochim Biophys Acta Mol Basis Dis.1865(7):1925-1937.
18. Kautz, L., Jung, G., Du, X., Gabayan, V., Chapman, J., Nasoff, M., Nemeth, E., & Ganz, T. (2015). Erythroferrone contributes to hepcidin suppression and iron overload in a mouse model of β-thalassemia. Blood, 126(17), 2031–2037.
19. Porter, J., Kattamis, A., & Cappellini, M. D. (Eds.). (2023). Iron overload: Pathophysiology, diagnosis and monitoring. In M. D. Cappellini (Eds.) et. al., Guidelines: For the Management of Transfusion Dependent Thalassaemia (TDT). (4th ed.). Thalassaemia International Federation.
20. Doltchinkova, V., Lozanova, S., Rukova, B., Nikolov, R., Ivanova, E., & Roumenin, C. (2023). Electrokinetic properties of healthy and β-thalassemia erythrocyte membranes under in vitro exposure to static magnetic field. Frontiers in chemistry, 11, 1197210.
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