EVALUATION OF GLUTATHIONE PEROXIDASE ACTIVITY, MALONYLALDEHYDE AND SELENIUM LEVELS IN SICKLE CELL ANAEMIA INDIVIDUALS ATTENDING NAUTH, NNEWI IN SOUTH-EASTERN NIGERIA.
DOI:
https://doi.org/10.61841/t39rrt42Keywords:
MDA Malonylaldehyde, GPx Glutathione peroxidase, Se Selenium SS Homozygous sickle cell hemoglobin , AA Heterozygous Adult hemoglobin , AS Heterozygous sickle disease carrier hemoglobin.Abstract
Background: Oxidative stress is an imbalance between the production and clearance of toxic free radicals known as reactive oxygen species (ROS). It is associated with hemolysis, a hallmark of SCD. SCD has long been recognized as an inflammatory condition and oxidative stress play important role in pathophysiology of SCA. Imbalance between production and elimination of reactive oxygen species (ROS) damages cell structures, including lipids, membranes, proteins and nucleic acids resulting in cell death or altered cell function.
Aim: The aim of this study was to measure the serum level of Glutathione peroxidase,
Malonaldehyde and Selenium in SCA (HbSS) in their steady state, AA (Healthy adult) and AS (sickle cell carriers)
Methods: This is a cross- sectional study. A total of one hundred and fifty aged matched participants were recruited for this study.50 SCA subjects with sickle cell anemia (SS). Glutathione peroxidase and Malonyaldehyde were measured using turbidometry and colorimetric methods respectively while Selenium was analysed using Atomic Absorption Spectrophotometry (AAS)
Results: The result of analysis of variance (ANOVA) showed that the mean serum level of MDA concentration (2.97±0.29) was higher in the SS group and was statistically significant (p< 0.05). MDA concentration was lower in the AS group. In the post hoc analysis MDA was statistically significant between SS vs AS and AA vs AA. The glutathione peroxidase activity was significantly lower in the SS group (0.85±0.12) compare with the mean values obtained in the AA and AS group. The GPx activity among the three groups was statistically significant while the post hoc analysis among the three groups showed statistical difference and was significant (p < 0.005) The Selenium levels in the SS group is lower compared with the values observed between the AA and AS group. The Se levels in the SS group was statistically lower (5.73±1.34) (p < 0.05) and showed significant difference. The comparison study between AS vs SS and AA vs AA were statistically significant.
Conclusion: The decrease in selenium level potentiates low and weakened antioxidant activity and capacity which also is a reflection of low level of glutathione peroxidase observed which is supposed to attack free radicals to prevent oxidative stress. The findings from this study are in tandem with other researches suggesting that the pathophysiology of sickle cell disease is associated with oxidative stress
References
Steinberg, M.H.; Adewoye, A.H. Modifier genes and sickle cell anemia. Current Opinion. Hematology (2006) 13 :131–136.
Hierso, R.; Waltz, X.; Mora, P.; Romana, M.; Lemonne, N.; Connes, P.; Hardy-Dessources, M.D. Effects of oxidative stress on red blood cell rheology in sickle cell patients. (2014) British. Journal Haematology 166 :601–606.
Kato, G.J.; Steinberg, M.H.; Gladwin, M.T. Intravascular hemolysis and the pathophysiology of sickle cell disease (2017). Journal of Clinical Investigation 1:12:750–760.
van Beers, E.J.; van Wijk, R. Oxidative stress in sickle cell disease; more than a DAMPsquib. Clinical Hemorheological. Microcirculation. (2018) 68 :239–250.
Jocelyne, A.M.V.; Pieme, C.A.; Chemegne, B.C.; Manonji, H.; Nono, B.L.N.; Mamiafo, C.T.;Moukette, B.M.; Nzufo, F.T.; Tazoacha, A (2016). Oxidative profile of sickle cell patients in a Cameroonian urban hospital. BMC Clinical Pathology 16:15.
Castilhos, L.G.; De Oliveira, J.S.; Adefegha, S.A.; Magni, L.P.; Doleski, P.H.; Abdalla, F.H.;De Andrade, C.M.; Leal, D.B.R (2017) Increased oxidative stress alters nucleosides metabolite levels in sickle cell anemia. Redox Representation. 222: 451–459.
Möckesch, B.; Connes, P.; Charlot, K.; Skinner, S.; Hardy-Dessources, M.-D.; Romana, M.;Jumet, S.; Petras, M.; Divialle-Doumdo, L.; Martin, C.; et al (2017) Association between oxidative stress and vascular reactivity in children with sickle cell anaemia and sickle haemoglobin C disease. British Journal of. Haematology. 178 :468–475.
Elias, D.B.D.; De Freitas, R.M.; Gonçalves, R.P.; Magalhães, H.Y.F.; De Sousa, J.H.;Magalhães, S.M.M. Evaluation of the concentration of malondialdehyde and nitrite in patients with sickle cell anemia treated or not with hydroxyurea. Einstein (Sao Paulo) (2010) 8: 414–418.
Emokpae, M.A.; Uadia, P.O. Association of oxidative stress markers with atherogenic index ofplasma in adult sickle cell nephropathy Anemia 2012, 2012, 767501 Antioxidants (2020) 9 863 13 of 15.
Lazzaretti, L.L.; Griebeler, I.H.; Manfredini, V.; Brandão, V.D.M.; Benfato, M.; Santin, A.P.;Wagner, S.; Castro, S.M.; Peralba, M.D.C. R (2008). Blood antioxidant parameters in sickle cell anemia patients in steady state. Journal of National Medicine Association.100 :897–902.
Biswal, S.; Rizwan, H.; Pal, S.; Sabnam, S.; Parida, P.; Pal, A. Oxidative stress, antioxidantcapacity, biomolecule damage, and inflammation symptoms of sickle cell disease in children (2018). Hematology 24, 1–9.
Renoux, C.; Joly, P.; Faës, C.; Mury, P.; Eglenen, B.; Turkay, M.; Yavas, G.; Yalcin, O.;Bertrand, Y.; Garnier, N.; et al (2018). Association between oxidative stress, genetic factors, and clinical severity in children with sickle cell anemia. Journal of Pediatric 195, 228–235.
Faës, C.; Balayssac-Siransy, E.; Connes, P.; Hivert, L.; Danho, C.; Bogui, P.; Martin, C.;Pialoux, V (2014) Moderate endurance exercise in patients with sickle cell anaemia: Effects on oxidative stress and endothelial activation. British Journal. Haematology. 164, 124–130.
Gammoh NZ, Rink L (2017). Zinc in infections and inflammation. Nutrients. 9:624
Hamdy MM, Mosallam DS, Jamal AM, Rabie WA (2015). Selenium and Vitamin E as antioxidants in chronic hemolytic anaemia. Are they deficient? A case control study in a group of Egyptian children. Journal of Advance research. 6:1071-1077.
16.He L, He T, Farrar S, Ji L, Liu T, Ma X (2017). Antioxidants maintain cellular redox homeostatsis by elimination of ROS. Cell Physiology Biochemistry. 44: 532-553.
Natta CL, Chen LC, Chow CK (1990). Selenium and glutathione peroxidase levels in SCA.
Acta Haematology. 83: 130-132.
Nnodim JK, Meludu SC, Dioka CE, Onah C, Ihim A, Atuegbu C (2014). Trace elements deficiency in patients with homozygous sickle cell disease. British Journal of Medical Research. Vol 4 pp3879- 3888.
Ranque B, Kitenge R, Ndiaye DD, et al. (2022) Estimating the risk of child mortality attributable to sickle cell anaemia in sub-Saharan Africa: a retrospective, multicenter, casecontrol study. Lancet Haematology 9:208.
Steinberg MH (1999). Management of sickle cell disease. National England Journal of Medicine. 340:1021-1030.
Sun Y, Ma A, Li Y,Han X, Wang Q, Liang H (2012). Vitamin E supplementation protects erythrocyte membranes from oxidative stress in healthy Chinese middle-aged and elderly people.
Nutritional Research. 32:328-332.
Thein MS, Igbineweka NE, Thein SL (2017). Sickle cell disease in the older adult.Pathology. 49:1-9.
Walter PB, Fung EB, Killilea DW, Jiang Q, Hudes M, Madden J et al (2006). Oxidativ stress and inflammation in iron overloaded patients with beta thalassaemias and sickle cell disease. British Journal of Haematology. 5(3): 135-254.
Whitehouse RC, Prasad AS, Rabbani PI, Cossaack ZT (1982). Zinc in plasma neutrophils,and erythrocytes as determined by flameless atomic absorption spectrophotometry.Clinical chemistry. 28:475-480.
Hebbel RP, Eaton JW, Balasingam M, Steinberg MH (1982). Spontaneous oxygen radical generation by sickle erythrocytes. Journal of clinical investigation. 70: 1253-1259.
Liao C, Hardison RC, Kennett MJ, Carlson BA, Paulson RF, Prabhuk S (2018).
Selenoproteins regulate stress erythroid progenitors and spleen microenvironment during stress erythropoiesis. Blood. 131:2568-2580.
Yubasiyan-Gurkan VA, Brewer GJ, Vander AJ, Guenther MJ, Prasad AS (1989). Net renal reabsorption of Zinc in healthy man and impaired handling in SCA. American Journal of Haematology. 31: 87-90.
Ursini F, Malorino M, Gregolin C (2018). The selenoenzyme, phospholipid hydroperoxide glutathione peroxidase. Biochimica et Biophysica Acta. 62-70.
Grossman and Wendel. Phospholipid, hydroperoxides are not substrates for seleniumdependent glutathione peroxidase. Book of Oxygen radicals in Chemistry and Biology.
Moris C R, Suh J H, Hagar W, Larkin S, Bland D A et al (2008). Erythrocyte glutaminedepletion altered redox environment and pulmonary hypertension in SCD. Blood 111, 402-410.
Downloads
Published
Issue
Section
License
Copyright (c) 2024 Wuraola Serah Nnaemeka, Madu Japhet Olisekodiaka, Anaelechi Jude Onuegbu, Chinawaeze John Aneke, Ejeatuluchukwu-alo Obi (Author)
This work is licensed under a Creative Commons Attribution 4.0 International License.
Licensing
Ninety Nine Publication publishes articles under the Creative Commons Attribution 4.0 International License (CC BY 4.0). This licensing allows for any use of the work, provided the original author(s) and source are credited, thereby facilitating the free exchange and use of research for the advancement of knowledge.
Detailed Licensing Terms
Attribution (BY): Users must give appropriate credit, provide a link to the license, and indicate if changes were made. Users may do so in any reasonable manner, but not in any way that suggests the licensor endorses them or their use.
No Additional Restrictions: Users may not apply legal terms or technological measures that legally restrict others from doing anything the license permits.
