Antioxidative Potential of Foetal Haemoglobin in Sickle Cell Disease

Yusuf Ishaya Dogonzo *

Department of Biochemistry, Federal University Ndufu Alike Ikwo (FUNAI), Ebonyi State, Nigeria.

Christopher Chimaobi Onyeabor

Department of Biochemistry, Federal University Ndufu Alike Ikwo (FUNAI), Ebonyi State, Nigeria.

Chiamaka Martha Oru

Department of Biochemistry, Federal University Ndufu Alike Ikwo (FUNAI), Ebonyi State, Nigeria.

Ogochukwu Dorothy Owusi

Department of Biochemistry, Federal University Ndufu Alike Ikwo (FUNAI), Ebonyi State, Nigeria.

Richard Chukwuebuka Ozor

Department of Biochemistry, Federal University Ndufu Alike Ikwo (FUNAI), Ebonyi State, Nigeria.

Otude Ebubechi

Department of Biochemistry, Federal University Ndufu Alike Ikwo (FUNAI), Ebonyi State, Nigeria.

Onyehara Esther Chizaram

Department of Biochemistry, Federal University Ndufu Alike Ikwo (FUNAI), Ebonyi State, Nigeria.

Oparaji Blessing

Department of Biochemistry, Federal University Ndufu Alike Ikwo (FUNAI), Ebonyi State, Nigeria.

*Author to whom correspondence should be addressed.


Abstract

Background: Oxidative stress is a clinical condition in sickle cell disease (SCD) that results from increased production of reactive oxygen species (ROS). High Foetal haemoglobin (HbF) is beneficial in sickle cell disease due to its ability to resist polymerization with sickle haemoglobin. The aim of this study is to determine the anti-oxidative potential of HbF in subjects with SCD.

Methods: Whole blood was used for the determination of HbF concentration while serum was used for the assay of Glutathione peroxidase (GPx), Super-oxide dismutase (SOD), and malondialdehyde (MDA). Alkali denaturation method was used for the determination of HbF while spectrophotometric method was used to assay for the various oxidative stress markers.

Results: The concentrations of HbF and MDA were significantly higher in the case subjects compared to the normal subjects. A direct relationship was observed between GPx (r = 0.47) and SOD (r = 0.46) with HbF. However, an inverse relationship was observed between MDA with HbF (r= -0.33), GPx (r= -0.18) and SOD (r= -0.26).

Conclusion: We conclude that HbF potentially associates with the antioxidant enzymes (GPx and SOD) to counteract the oxidative effect of ROS in SCD.

Keywords: Sickle cell disease, foetal haemoglobin, oxidative stress, lipid peroxidation, glutathione peroxidise, super oxide dismutase


How to Cite

Dogonzo , Yusuf Ishaya, Christopher Chimaobi Onyeabor, Chiamaka Martha Oru, Ogochukwu Dorothy Owusi, Richard Chukwuebuka Ozor, Otude Ebubechi, Onyehara Esther Chizaram, and Oparaji Blessing. 2023. “Antioxidative Potential of Foetal Haemoglobin in Sickle Cell Disease”. International Journal of Research and Reports in Hematology 6 (2):179-84. https://journalijr2h.com/index.php/IJR2H/article/view/121.

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References

Piel FB, Steinberg MH, Rees DC. Sickle cell disease. N Engl J Med. 2017;376(16): 1561-1573.

Antwi-Boasiako C, Dankwah GB, Aryee R, Heyfron-Benjamin C, Dankor ES & Campbell AD. Oxidative Profile of Patients with Sickle Cell Disease. Medical Sciences. 2019;7(2):17.

Edwards O, Burris A, Lua J, Wilkie DJ, Ezenwa MO, Doré S. Influence of haptoglobin polymorphism on stroke in sickle cell disease patients. Genes. 2022; 13(1):144.

Vona R, Sponsi NM, Mattia L, Gambardella L, Straface E, Pietraforte D. Sickle Cell Disease: Role of oxidative stress and antioxidant therapy. Antioxidant. 2021;10(2):296.

Afolayan JA, Adekile AD, Ogunrinde GO. Serum malondialdehyde and total antioxidant status in adult sickle cell disease patients in steady state. African Health Sciences. 2019;19(3):2649-2656.

Dalle-Donne I, Rossi R, Colombo R, Giustarini D, Milzani A. Biomarkers of oxidative damage in human disease. Clinical Chemistry. 2006;52(4): 601-623.

Baliga S, Chaudhary M, Bhansali P, Agrawal A, Gundawar S. Estimation of MDA levels in serum and saliva of children affected with SCA. J indian Soc Pedod Prev Dent. 2018;36(1):43-47.

Atiku SM, Loiise N, Kasozi DM. Severe oxidative stress in SCD patients with uncomplicated plasmodium falciparum malaria in kampala Uganda. Bmc Infect Dis. 2019;19:600.

Erhabor O, Jiya N, Abubakar M, Usman S. Some antioxidant enzymes among children with Sickle Cell Disease attending Usmanu Danfodio University teaching Hospital Sokoto, North Western Nigeria. Journal of Blood Diseases. 2019;9:60-76.

Poli G, Leonarduzzi G, Biasi F, Chiarpotto E. Oxidative stress and cell signalling. Current Medicinal Chemistry. 2004;11(9):1163-1182.

Kaufman DP, Khattar J, Lappin SL. Physiology, fetal hemoglobin. StatPearls Publishing; 2023.

Collela MP, Traina F. Fetal haemoglobin and hemolysis markers in sickle cell anemia. Brazilian Journal of Hematology and Hemotherapy. 2015;37(3):143-9.

Crossley M, Christakopoulos GE & Weiss MJ. Effective therapies for sickle cell disease: Are we there yet? Trends Genetics. 2022;38(12):1284-1298

Egesa WI, Nakalema G, Waibi WM, Turyasiima M, Amuje E, Kiconco G, et al. Sickle cell disease in children and adolescents: A review of the historical, clinical, and public health perspective of sub-saharan Africa and beyond. International Journal of Pediatrics. 2022; 8:3885979.

Dogonzo IY, Ekoh OC, Enewor TN. Under reported potentials of low foetal haemoglobin in sickle cell disease. Int J Blood Res Disord. 2022;9:080.

Akinsheye I, Alsultan A, Solovieff N, Ngo D, Baldwin CT, Sebastiani P, Chui DH, Steinberg MH. Blood. 2011;118(1):19-27.

Sales RR, Nogueira BL, Tosatti JAG, Gomes KB, Luizon MR. Do genetic polymorphisms affect fetal hemoglobin (HbF) levels in patients with sickle cell anemia treated with hydroxyurea? A systematic review and pathway analysis. Frontiers in Pharmacology. 2022; 12:779497.

Olaniyi JA, Arinola OG, Odetunde AB. Foetal haemoglobin (HbF) status in adult sickle cell anaemia patients in Ibadan, Nigeria. Annals of Ibadan Postgraduate Medicine. 2010;8(1):30-33.

Nur E, Biemond BJ, Otten HM, Brandjes DP, Schnog JJB & CURAMA Study Group. Oxidative stress in sickle cell disease; pathophysiology and potential implications for disease management. American Journal of Hematology. 2011;86(6):484-489.

Nader E, Grau M, Fort R, Collins B, Cannas G, Gauthier A. Connes P. Hydroxyurea therapy modulates sickle cell anemia red blood cell physiology: Impact on RBC deformability, oxidative stress, nitrite levels and nitric oxide synthase signalling pathway. Nitric Oxide. 2018;81: 28-35

Okorie CP, Nwagha T, Ejezie F. Assessment of some indicators of oxidative stress in nigerian sickle cell anemic patients. Ann Afr Med. 2018;17(1): 11–16.

Vona R, Sposi NM, Mattia L, Gambardella L, Straface E, Pietraforte D. Sickle cell disease: Role of Oxidative Stress and Antioxidant Therapy. Antioxidants. 2021; 2(10):296.

Biswal S, Rizwan H, Pal S, Sabnam S, Parida P, Pal A. Oxidative stress, antioxidant capacity, biomolecule damage, and inflammation symptoms of sickle cell disease in children. Hematology 2019; 24(1):1-9.

Moreira JA, Laurentino MR, Machado RP, Barbosa MC, Goncalves RP, Mota AM et al. Pattern of haemolysis parameters and association with fetal hemoglobin in sickle cell anemia patients in steady state. Brazilian Journal of Hematology and Hemotherapy. 2015;37(3):167-171.

Lia B, Zhua X, Wardb CM, Starlard-Davenport A, Takezakia M, Berryd A, et al. MIR-144-mediated NRF2 gene silencing inhibits fetal hemoglobin expression in sickle cell disease. Experimental Hematology. 2019;70: 85−96.e5.

Zhu X, Oseghale AR, Nicole LH, Li B, Pace BS. Mechanisms of NRF2 activation to mediate fetal haemoglobin induction and protection against oxidative stress in sickle cell disease. Experimental Biology and Medicine. 2019;244(2):171–182.