Assessment of Lipid Peroxidation and Antioxidant Status in Common Haemoglobin Phenotypes in Osun State, Southwestern Nigeria
Background: Generally speaking, erythrocyte haemoglobin (Hb) is pro-oxidant in nature constantly generating superoxide (O2˙ˉ) species in biological system of all Hb phenotypes. Sometimes, this reactive oxygen species (ROS) triggers lipid peroxidation with eventual rise in oxidative stress, particularly when the supposed self-sustaining antioxidant defence system is overwhelmed. Worse still, abnormal Hb generates multiple of O2˙ˉ specie. Recent evidence has linked abnormal haemoglobins S and C in sickle cell diseases (SCD) to various complications with multiple pro-oxidant processes; however, similar studies in relation with abnormal haemoglobin traits are sparse. More so, reports on rate of activities of various antioxidant enzymes in SCDs are still contradictory. This study aimed to assess interplay between lipid peroxidation and antioxidant defence capacity in various haemoglobin variants.
Method: A total number of 150 participants with different haemoglobin variants were recruited. Plasma levels of malondialdehyde (MDA), total antioxidant status (TAS), superoxide dismutase (SOD) and glutathione peroxidase (GPx) enzymes were assayed using spectrophotometric method.
Result: The results showed that plasma levels of MDA and erythrocytic SOD were significantly increased (P<0.05) in abnormal haemoglobins in that order of HbSS >HbSC >HbAC >HbAS, when compared with controls (HbAA). Conversely, plasma levels of GPx and TAS showed significant reductions (p<0.05), respectively.
Conclusion: The results suggest that both sickle cell diseases and the carriers were relatively more vulnerable to systemic oxidative stress (in that order of HbSS> HbSC > HbAC >HbAS) contrary to normal haemoglobin phenotype, possibly owing to ineffective antioxidant mechanisms needed for keeping spontaneous generation of free radicals in control.
Kuhn V, Diederich L, Keller TCS IV, Kramer CM, Lückstädt W, Panknin C, et al. Antioxidants & Redox Signaling. 2017; 26(13):718-42. doi.org/10.1089/ars.2016.6954.
Hathazi D, Scurtu F, Bischin C, Mot A, Attia AAA, Kongsted J, et al. The Reaction of Oxy Hemoglobin with Nitrite: Mechanism, Antioxidant-Modulated Effect, and Implications for Blood Substitute Evaluation. Molecules. 2018;23:350. DOI: 10.3390/molecules23020350.
Klings ES and Farber HW. Role of free radicals in the pathogenesis of acute chest syndrome in sickle cell disease. Respiratory Research. 2001;2:280–5.
Lang E, Qadri SM, Zelenak C, Gu S, Rotte A, Draeger A, Lang F. Inhibition of suicidal erythrocyte death by blebbistatin. American journal of physiology. Cell physiology. 2011;301:C490–C498.
Chaves MA, Leonart MS, do Nascimento AJ. Oxidative process in erythrocytes of individuals with haemoglobin S. Hematology 2008;13:187–92.
Key NS, Connes P, Derebail VK. Negative Health Implications Of Sickle Cell Trait in High Income Countries: From The Football Field To The Laboratory. British Journal of Haematology. 2015;170(1):5–14. DOI:10.1111/bjh.13363.
Dasgupta T, Hebbel RP, Kaul DK. Protective effect of arginine on oxidative stress in transgenic sickle mouse models. Free Radical Biology and Medicine. 2006;41:1771–80.
Alsultan AI, Seif MA, Amin TT, Naboli M, Alsuliman AM. Relationship between oxidative stress, ferritin and insulin resistance in sickle cell disease. European Review for Medical and Pharmacological Sciences. 2010;14: 527–38.
Koracevic D, Koracevic G, Djordjevie V, Andrejevic S, Cosic V. Method for the measurement of antioxidant activity in human fluids. J. Clin. Pathol. 2001;54:356–61.
Gutteridge JM, Wilkins S. Copper –dependent hydroxyl radical damage to ascorbic acid. FEBS Letters. 1982;137:329.
Rotruck JT, Pope AL, Ganther HE, Swanson AB, Hafeman DG, Hoekstra WG. Selenium: Biochemical role as a component of glutathione peroxidase. Science. 1973;179:588-90.
Misra HP, Fridovich I. Determination of Superoxide dismutase. Journal of biological chemistry. 1972;247:3170-5.
Prakash A. Antioxidant Activity. Medallion Laboratories Analytical Progress. 2001;19(2).
Abiodun MA, Uadia PO, Kuliya GA. Antioxidant Enzymes and Acute Phase Proteins Correlate with Marker of Lipid Peroxide in Adult Nigerian Sickle Cell Disease Patients. Iranian Journal of Basic Medical Sciences. 2010;13:177–82.
Ama Moor VJ, Pieme CA, Chemegne BC, Manonji H, Nono BLN, Mamiafo CT, et al. Oxidative profile of sickle cell patients in a Cameroonian urban hospital. BMC Clinical Pathology. 2016; 16:15. http://doi.org/10.1186/s12907-016-0037-5.
Alvarez O, Montague NS, Marin M, O'Brien R, Rodriguez MM. Quantification of Sickle Cells in the Peripheral Smear as a Marker of Disease Severity, Fetal and Pediatric Pathology, 2015;34:(3)149-54, DOI:10.3109/15513815.2014.987937.
Titus J, Chari S, Gupta M, Parekh N. Pro–oxidant and anti–oxidant status in patients of sickle cell anemia. Indian Journal of Clinical Biochemistry. 2004;19(2):168–72.
Manfredini V, Lazzaretti LL, Griebeler IH, Santin AP, Brandão VD, Wagner S, et al. Blood antioxidant parameters in sickle cell anemia patients in steady state. Original communications. Journal of the National Medical Association. 2008;100(8):897–902.
Luzzatto L. Sterile ‘abscess’ of the spleen and the sickle cell trait. Mediterranean Journal of Hematology and Infectious Diseases. 2018;10(1):e2018003. DOI: 10.4084/MJHID.2018.003.
Connes P, Hardy-Dessources, MD, Hue O. Counterpoint: Sickle cell trait should not be considered asymptomatic and as a benign condition during physical activity. Journal of Applied Physiology. 2007;103:2140–1.
Tsaras G, Owusu-Ansah A, Boateng FO, Amoateng-Adjepong Y. Complications associated with sickle cell trait: a brief narrative review. American Journal of Medicine. 2009;122(6):507-12. DOI:10.1016/j.amjmed.2008.12.020.
Chirico E. The role of exercise training on oxidative stress and inammation in vascular diseases. Human health and pathology. 2012;83-86. (Accessed 17 March, 2018).
Prakash H, Adinath S, Aarti K, Rahul G, Maya V. Antioxidant Status and Lipid Peroxidation in Sickle Cell Anaemia. Biomedical Research. 2010;21(4):461–4.
Hongmei R, Ghebremeskel K, Okpala. Patients with sickle cell anaemia have reduced antioxidant production. International Journal for Vitamin and Nutrition Research. 2008;78:139–47.
Kohne E. Hemoglobinopathies: clinical manifestations, diagnosis, and treatment. Deutsches Ärzteblatt International. 2011;108:532–40.
Scott MD, Eaton JW, Chiu DT-Y, Kuypers FA, Lubin B. Enhancement of the erythrocyte superoxide dismutase activity: effect on cellular oxidant defense. Blood. 1989;74:2542–9.
Arinola OG, Olaniyi SA, Akibinu MO. Evaluation of antioxidant levels and trace elements status in Nigerian sickle cell disease patients with plasmodium parasitae-mia. Pakistan Journal of Nutrition. 2008;7(6):766–69.
Foluke F, Kayode A, Johan A, Modupe K. Total anti-oxidant status in sickle cell disease patients in steady state. Journal of the National Medical Association. 2008;100(8):891-4.
Naeim F, Rao PN, Song SX, Grod WW. Disorders of Red Blood Cells—Anemias. In: Naeim F, editor. Atlas of Hematopathology : Morphology, Immunophenotype, Cytogenetics, and Molecular Approaches, 1st ed. USA: Academic Press; 2013. p.675–704.
Kato GJ, Steinberg MH, Gladwin MT. Intravascular hemolysis and the pathophysiology of sickle cell disease. The Journal of Clinical Investigation. 2017;127(3):750-60. DOI:10.1172/JCI89741.
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