Skip to main content
Top
Published in: Annals of Hematology 4/2012

01-04-2012 | Original Article

Oxidative stress and antioxidant capacity in sickle cell anaemia patients receiving different treatments and medications for different periods of time

Authors: Edis Belini Junior, Danilo Grünig Humberto da Silva, Lidiane de Souza Torres, Eduardo Alves de Almeida, Rodolfo Delfini Cancado, Carlos Chiattone, Claudia Regina Bonini-Domingos

Published in: Annals of Hematology | Issue 4/2012

Login to get access

Abstract

To evaluate, in a longitudinal study, the profile of lipid peroxidation and antioxidant capacity markers in sickle cell anaemia patients receiving different treatments and medication over different time periods. The three groups were: patients undergoing transfusion therapy and receiving iron chelator deferasirox (DFX group, n = 20); patients receiving deferasirox and hydroxyurea (DFX + HU group, n = 10), and patients receiving only folic acid (FA group, n = 15). Thiobarbituric acid-reactive substance (TBARS) assays and trolox-equivalent antioxidant capacity (TEAC) assays were evaluated during two different periods of analysis, T0 and T1 (after ~388 days). Higher FA group TBARS values were observed compared with the DFX + HU group (p = 0.016) at T0; and at T1, higher FA group TBARS values were also observed compared with both the DFX group (p = 0.003) and the DFX + HU group (p = 0.0002). No variation in TEAC values was seen between groups, at either T0 or T1. The mean values of TBARS and TEAC for both the DFX and DFX + HU groups decreased at T1. The antioxidant effects of HU and DFX were observed by through an increase in TEAC levels in DFX and DFX + HU groups when compared with those of normal subjects. Increased TEAC values were not recorded in the FA group, and lipid peroxidation was seen to decrease after DFX and HU use.
Literature
1.
go back to reference Weatherall D, Hofman K, Rodgers G, Ruffin J, Hrynkow S (2005) A case for developing north–south partnerships for research in sickle cell disease. Blood 105:921–923PubMedCrossRef Weatherall D, Hofman K, Rodgers G, Ruffin J, Hrynkow S (2005) A case for developing north–south partnerships for research in sickle cell disease. Blood 105:921–923PubMedCrossRef
2.
go back to reference Bunn HF (1997) Mechanisms of disease—pathogenesis and treatment of sickle cell disease. N Engl J Med 337:762–769PubMedCrossRef Bunn HF (1997) Mechanisms of disease—pathogenesis and treatment of sickle cell disease. N Engl J Med 337:762–769PubMedCrossRef
4.
go back to reference Vekilov PG (2007) Sickle-cell haemoglobin polymerization: is it the primary pathogenic event of sickle-cell anaemia? Br J Haematol 139:173–184PubMedCrossRef Vekilov PG (2007) Sickle-cell haemoglobin polymerization: is it the primary pathogenic event of sickle-cell anaemia? Br J Haematol 139:173–184PubMedCrossRef
5.
go back to reference Repka T, Hebbel RP (1991) Hydroxyl radical formation by sickle erythrocyte-membranes—role of pathological iron deposits and cytoplasmic reducing agents. Blood 78:2753–2758PubMed Repka T, Hebbel RP (1991) Hydroxyl radical formation by sickle erythrocyte-membranes—role of pathological iron deposits and cytoplasmic reducing agents. Blood 78:2753–2758PubMed
6.
go back to reference Reiter CD, Wang X, Tanus-Santos JE, Hogg N, Cannon RO III, Schechter AN et al (2002) Cell-free hemoglobin limits nitric oxide bioavailability in sickle-cell disease. Nat Med 8:1383–1389PubMedCrossRef Reiter CD, Wang X, Tanus-Santos JE, Hogg N, Cannon RO III, Schechter AN et al (2002) Cell-free hemoglobin limits nitric oxide bioavailability in sickle-cell disease. Nat Med 8:1383–1389PubMedCrossRef
7.
go back to reference Kato GJ, Hebbel RP, Steinberg MH, Gladwin MT (2009) Vasculopathy in sickle cell disease: biology, pathophysiology, genetics, translational medicine, and new research directions. Am J Hematol 84:618–625PubMedCrossRef Kato GJ, Hebbel RP, Steinberg MH, Gladwin MT (2009) Vasculopathy in sickle cell disease: biology, pathophysiology, genetics, translational medicine, and new research directions. Am J Hematol 84:618–625PubMedCrossRef
8.
go back to reference Wood KC, Hebbel RP, Granger DN (2005) Endothelial cell NADPH oxidase mediates the cerebral microvascular dysfunction in sickle cell transgenic mice. FASEB J 19:989–991PubMed Wood KC, Hebbel RP, Granger DN (2005) Endothelial cell NADPH oxidase mediates the cerebral microvascular dysfunction in sickle cell transgenic mice. FASEB J 19:989–991PubMed
9.
go back to reference Belcher JD, Mahaseth H, Welch TE, Vilback AE, Sonbol KM, Kalambur VS et al (2005) Critical role of endothelial cell activation in hypoxia-induced vasoocclusion in transgenic sickle mice. Am J Physiol Heart Circ Physiol 288:H2715–H2725PubMedCrossRef Belcher JD, Mahaseth H, Welch TE, Vilback AE, Sonbol KM, Kalambur VS et al (2005) Critical role of endothelial cell activation in hypoxia-induced vasoocclusion in transgenic sickle mice. Am J Physiol Heart Circ Physiol 288:H2715–H2725PubMedCrossRef
10.
go back to reference Belcher JD, Bryant CJ, Nguyen J, Bowlin PR, Kielbik MC, Bischof JC et al (2003) Transgenic sickle mice have vascular inflammation. Blood 101:3953–3959PubMedCrossRef Belcher JD, Bryant CJ, Nguyen J, Bowlin PR, Kielbik MC, Bischof JC et al (2003) Transgenic sickle mice have vascular inflammation. Blood 101:3953–3959PubMedCrossRef
11.
go back to reference Frenette PS (2002) Sickle cell vaso-occlusion: multistep and multicellular paradigm. Curr Opin Hematol 9:101–106PubMedCrossRef Frenette PS (2002) Sickle cell vaso-occlusion: multistep and multicellular paradigm. Curr Opin Hematol 9:101–106PubMedCrossRef
12.
go back to reference Conran N, Franco-Penteado CF, Costa FF (2009) Newer aspects of the pathophysiology of sickle cell disease vaso-occlusion. Hemoglobin 33:1–16PubMedCrossRef Conran N, Franco-Penteado CF, Costa FF (2009) Newer aspects of the pathophysiology of sickle cell disease vaso-occlusion. Hemoglobin 33:1–16PubMedCrossRef
14.
go back to reference Covas DT, de Lucena Angulo I, Vianna Bonini PP, Zago MA (2004) Effects of hydroxyurea on the membrane of erythrocytes and platelets in sickle cell anemia. Haematologica 89:273–280PubMed Covas DT, de Lucena Angulo I, Vianna Bonini PP, Zago MA (2004) Effects of hydroxyurea on the membrane of erythrocytes and platelets in sickle cell anemia. Haematologica 89:273–280PubMed
15.
go back to reference Kinney TR, Helms RW, O’Branski EE, Ohene-Frempong K, Wang W, Daeschner C et al (1999) Safety of hydroxyurea in children with sickle cell anemia: results of the HUG-KIDS study, a phase I/II trial. Pediatric Hydroxyurea Group. Blood 94:1550–1554PubMed Kinney TR, Helms RW, O’Branski EE, Ohene-Frempong K, Wang W, Daeschner C et al (1999) Safety of hydroxyurea in children with sickle cell anemia: results of the HUG-KIDS study, a phase I/II trial. Pediatric Hydroxyurea Group. Blood 94:1550–1554PubMed
16.
go back to reference Schnog JB, Duits AJ, Muskiet FA, ten Cate H, Rojer RA, Brandjes DP (2004) Sickle cell disease; a general overview. Neth J Med 62:364–374PubMed Schnog JB, Duits AJ, Muskiet FA, ten Cate H, Rojer RA, Brandjes DP (2004) Sickle cell disease; a general overview. Neth J Med 62:364–374PubMed
17.
go back to reference Halsey C, Roberts IAG (2003) The role of hydroxyurea in sickle cell disease. Br J Haematol 120:177–186PubMedCrossRef Halsey C, Roberts IAG (2003) The role of hydroxyurea in sickle cell disease. Br J Haematol 120:177–186PubMedCrossRef
18.
go back to reference Hillery CA, Du MC, Wang WC, Scott JP (2000) Hydroxyurea therapy decreases the in vitro adhesion of sickle erythrocytes to thrombospondin and laminin. Br J Haematol 109:322–327PubMedCrossRef Hillery CA, Du MC, Wang WC, Scott JP (2000) Hydroxyurea therapy decreases the in vitro adhesion of sickle erythrocytes to thrombospondin and laminin. Br J Haematol 109:322–327PubMedCrossRef
19.
go back to reference Lou TF, Singh M, Mackie A, Li W, Pace BS (2009) Hydroxyurea generates nitric oxide in human erythroid cells: mechanisms for gamma-globin gene activation. Exp Biol Med 234:1374–1382CrossRef Lou TF, Singh M, Mackie A, Li W, Pace BS (2009) Hydroxyurea generates nitric oxide in human erythroid cells: mechanisms for gamma-globin gene activation. Exp Biol Med 234:1374–1382CrossRef
20.
go back to reference Adams RJ, Mckie VC, Hsu L, Files B, Vichinsky E, Pegelow C et al (1998) Prevention of a first stroke by transfusions in children with sickle, cell anemia and abnormal results on transcranial Doppler ultrasonography. N Engl J Med 339:5–11PubMedCrossRef Adams RJ, Mckie VC, Hsu L, Files B, Vichinsky E, Pegelow C et al (1998) Prevention of a first stroke by transfusions in children with sickle, cell anemia and abnormal results on transcranial Doppler ultrasonography. N Engl J Med 339:5–11PubMedCrossRef
21.
go back to reference Vichinsky E, Butensky E, Fung E, Hudes M, Theil E, Ferrell L et al (2005) Comparison of organ dysfunction in transfused patients with SCD or beta thalassemia. Am J Hematol 80:70–74PubMedCrossRef Vichinsky E, Butensky E, Fung E, Hudes M, Theil E, Ferrell L et al (2005) Comparison of organ dysfunction in transfused patients with SCD or beta thalassemia. Am J Hematol 80:70–74PubMedCrossRef
22.
go back to reference Cappellini MD, Porter J, El-Beshlawy A, Li CK, Seymour JF, Elalfy M et al (2010) Tailoring iron chelation by iron intake and serum ferritin: the prospective EPIC study of deferasirox in 1744 patients with transfusion-dependent anemias. Haematologica 95:557–566PubMedCrossRef Cappellini MD, Porter J, El-Beshlawy A, Li CK, Seymour JF, Elalfy M et al (2010) Tailoring iron chelation by iron intake and serum ferritin: the prospective EPIC study of deferasirox in 1744 patients with transfusion-dependent anemias. Haematologica 95:557–566PubMedCrossRef
23.
go back to reference Steinberg MH (2008) Sickle cell anemia, the first molecular disease: overview of molecular etiology, pathophysiology, and therapeutic approaches. Scientific World Journal 8:1295–1324PubMedCrossRef Steinberg MH (2008) Sickle cell anemia, the first molecular disease: overview of molecular etiology, pathophysiology, and therapeutic approaches. Scientific World Journal 8:1295–1324PubMedCrossRef
24.
go back to reference Bonini-Domingos CR (2006) Metodologias laboratoriais para o diagnóstico de hemoglobinopatias e talassemias. NH, São José do Rio Preto Bonini-Domingos CR (2006) Metodologias laboratoriais para o diagnóstico de hemoglobinopatias e talassemias. NH, São José do Rio Preto
25.
go back to reference Belini E, Cancado RD, Domingos CRB (2010) The Xmnl polymorphic site 5′ to the gene G gamma in a Brazilian patient with sickle cell anaemia—fetal haemoglobin concentration, haematology and clinical features. Arch Med Sci 6:822–825CrossRef Belini E, Cancado RD, Domingos CRB (2010) The Xmnl polymorphic site 5′ to the gene G gamma in a Brazilian patient with sickle cell anaemia—fetal haemoglobin concentration, haematology and clinical features. Arch Med Sci 6:822–825CrossRef
26.
go back to reference Sutton M, Bouhassira EE, Nagel RL (1989) Polymerase chain-reaction amplification applied to the determination of beta-like globin gene-cluster haplotypes. Am J Hematol 32:66–69PubMedCrossRef Sutton M, Bouhassira EE, Nagel RL (1989) Polymerase chain-reaction amplification applied to the determination of beta-like globin gene-cluster haplotypes. Am J Hematol 32:66–69PubMedCrossRef
27.
go back to reference Ondei LS, Silveira LM, Leite AA, Souza DR, Pinhel MA, Percario S et al (2009) Lipid peroxidation and antioxidant capacity of G6PD-deficient patients with A-(202G>A) mutation. Genet Mol Res 8:1345–1351PubMedCrossRef Ondei LS, Silveira LM, Leite AA, Souza DR, Pinhel MA, Percario S et al (2009) Lipid peroxidation and antioxidant capacity of G6PD-deficient patients with A-(202G>A) mutation. Genet Mol Res 8:1345–1351PubMedCrossRef
28.
go back to reference Uchiyama M, Mihara M (1978) Determination of malonaldehyde precursor in tissues by thiobarbituric acid test. Anal Biochem 86:271–278PubMedCrossRef Uchiyama M, Mihara M (1978) Determination of malonaldehyde precursor in tissues by thiobarbituric acid test. Anal Biochem 86:271–278PubMedCrossRef
29.
go back to reference Miller NJ, Riceevans C, Davies MJ, Gopinathan V, Milner A (1993) A novel method for measuring antioxidant capacity and its application to monitoring the antioxidant status in premature neonates. Clin Sci 84:407–412PubMed Miller NJ, Riceevans C, Davies MJ, Gopinathan V, Milner A (1993) A novel method for measuring antioxidant capacity and its application to monitoring the antioxidant status in premature neonates. Clin Sci 84:407–412PubMed
30.
go back to reference Re R, Pellegrini N, Proteggente A, Pannala A, Yang M, Rice-Evans C (1999) Antioxidant activity applying an improved ABTS radical cation decolorization assay. Free Radic Biol Med 26:1231–1237PubMedCrossRef Re R, Pellegrini N, Proteggente A, Pannala A, Yang M, Rice-Evans C (1999) Antioxidant activity applying an improved ABTS radical cation decolorization assay. Free Radic Biol Med 26:1231–1237PubMedCrossRef
31.
go back to reference Manfredini V, Lazzaretti LL, Griebeler IH, Santin AP, Brandao VDM, Wagner S et al (2008) Blood antioxidant parameters in sickle cell anemia patients in steady state. J Natl Med Assoc 100:897–902PubMed Manfredini V, Lazzaretti LL, Griebeler IH, Santin AP, Brandao VDM, Wagner S et al (2008) Blood antioxidant parameters in sickle cell anemia patients in steady state. J Natl Med Assoc 100:897–902PubMed
32.
go back to reference Jain SK, Ross JD, Levy GJ, Duett J (1990) The effect of malonyldialdehyde on viscosity of normal and sickle red blood cells. Biochem Med Metab Biol 44:37–41PubMedCrossRef Jain SK, Ross JD, Levy GJ, Duett J (1990) The effect of malonyldialdehyde on viscosity of normal and sickle red blood cells. Biochem Med Metab Biol 44:37–41PubMedCrossRef
33.
go back to reference Sertac A, Bingol F, Aydin S, Uslu A (1997) Peroxidative damage in sickle-cell erythrocyte ghosts: protective effect of allopurinol. Gen Pharmacol 28:427–428PubMedCrossRef Sertac A, Bingol F, Aydin S, Uslu A (1997) Peroxidative damage in sickle-cell erythrocyte ghosts: protective effect of allopurinol. Gen Pharmacol 28:427–428PubMedCrossRef
34.
go back to reference Walter PB, Fung EB, Killilea DW, Jiang Q, Hudes M, Madden J et al (2006) Oxidative stress and inflammation in iron-overloaded patients with beta-thalassaemia or sickle cell disease. Br J Haematol 135:254–263PubMedCrossRef Walter PB, Fung EB, Killilea DW, Jiang Q, Hudes M, Madden J et al (2006) Oxidative stress and inflammation in iron-overloaded patients with beta-thalassaemia or sickle cell disease. Br J Haematol 135:254–263PubMedCrossRef
35.
go back to reference Wood KC, Granger DN (2007) Sickle cell disease: role of reactive oxygen and nitrogen metabolites. Clin Exp Pharmacol Physiol 34:926–932PubMedCrossRef Wood KC, Granger DN (2007) Sickle cell disease: role of reactive oxygen and nitrogen metabolites. Clin Exp Pharmacol Physiol 34:926–932PubMedCrossRef
36.
go back to reference Aslan M, Ryan TM, Adler B, Townes TM, Parks DA, Thompson JA et al (2001) Oxygen radical inhibition of nitric oxide-dependent vascular function in sickle cell disease. Proc Natl Acad Sci USA 98:15215–15220PubMedCrossRef Aslan M, Ryan TM, Adler B, Townes TM, Parks DA, Thompson JA et al (2001) Oxygen radical inhibition of nitric oxide-dependent vascular function in sickle cell disease. Proc Natl Acad Sci USA 98:15215–15220PubMedCrossRef
37.
go back to reference Hebbel RP, Eaton JW, Balasingam M, Steinberg MH (1982) Spontaneous oxygen radical generation by sickle erythrocytes. J Clin Invest 70:1253–1259PubMedCrossRef Hebbel RP, Eaton JW, Balasingam M, Steinberg MH (1982) Spontaneous oxygen radical generation by sickle erythrocytes. J Clin Invest 70:1253–1259PubMedCrossRef
38.
go back to reference Landburg PP, Teerlink T, Biemond BJ, Brandjes DP, Muskiet FA, Duits AJ et al (2010) Plasma asymmetric dimethylarginine concentrations in sickle cell disease are related to the hemolytic phenotype. Blood Cells Mol Dis 44:229–232PubMedCrossRef Landburg PP, Teerlink T, Biemond BJ, Brandjes DP, Muskiet FA, Duits AJ et al (2010) Plasma asymmetric dimethylarginine concentrations in sickle cell disease are related to the hemolytic phenotype. Blood Cells Mol Dis 44:229–232PubMedCrossRef
39.
go back to reference Xia Y, Dawson VL, Dawson TM, Snyder SH, Zweier JL (1996) Nitric oxide synthase generates superoxide and nitric oxide in arginine-depleted cells leading to peroxynitrite-mediated cellular injury. Proc Natl Acad Sci USA 93:6770–6774PubMedCrossRef Xia Y, Dawson VL, Dawson TM, Snyder SH, Zweier JL (1996) Nitric oxide synthase generates superoxide and nitric oxide in arginine-depleted cells leading to peroxynitrite-mediated cellular injury. Proc Natl Acad Sci USA 93:6770–6774PubMedCrossRef
40.
go back to reference Morris CR, Kato GJ, Poljakovic M, Wang X, Blackwelder WC, Sachdev V et al (2005) Dysregulated arginine metabolism, hemolysis-associated pulmonary hypertension, and mortality in sickle cell disease. JAMA 294:81–90PubMedCrossRef Morris CR, Kato GJ, Poljakovic M, Wang X, Blackwelder WC, Sachdev V et al (2005) Dysregulated arginine metabolism, hemolysis-associated pulmonary hypertension, and mortality in sickle cell disease. JAMA 294:81–90PubMedCrossRef
41.
go back to reference Amer J, Ghoti H, Rachmilewitz E, Koren A, Levin C, Fibach E (2006) Red blood cells, platelets and polymorphonuclear neutrophils of patients with sickle cell disease exhibit oxidative stress that can be ameliorated by antioxidants. Br J Haematol 132:108–113PubMedCrossRef Amer J, Ghoti H, Rachmilewitz E, Koren A, Levin C, Fibach E (2006) Red blood cells, platelets and polymorphonuclear neutrophils of patients with sickle cell disease exhibit oxidative stress that can be ameliorated by antioxidants. Br J Haematol 132:108–113PubMedCrossRef
42.
go back to reference Schacter L, Warth JA, Gordon EM, Prasad A, Klein BL (1988) Altered amount and activity of superoxide dismutase in sickle cell anemia. FASEB J 2:237–243PubMed Schacter L, Warth JA, Gordon EM, Prasad A, Klein BL (1988) Altered amount and activity of superoxide dismutase in sickle cell anemia. FASEB J 2:237–243PubMed
43.
go back to reference Hebbel RP, Osarogiagbon R, Kaul D (2004) The endothelial biology of sickle cell disease: inflammation and a chronic vasculopathy. Microcirculation 11:129–151PubMedCrossRef Hebbel RP, Osarogiagbon R, Kaul D (2004) The endothelial biology of sickle cell disease: inflammation and a chronic vasculopathy. Microcirculation 11:129–151PubMedCrossRef
44.
go back to reference Cighetti G, Duca L, Bortone L, Sala S, Nava I, Fiorelli G et al (2002) Oxidative status and malondialdehyde in beta-thalassaemia patients. Eur J Clin Invest 32:55–60PubMedCrossRef Cighetti G, Duca L, Bortone L, Sala S, Nava I, Fiorelli G et al (2002) Oxidative status and malondialdehyde in beta-thalassaemia patients. Eur J Clin Invest 32:55–60PubMedCrossRef
45.
go back to reference Hebbel RP, Morgan WT, Eaton JW, Hedlund BE (1988) Accelerated autoxidation and heme loss due to instability of sickle hemoglobin. Proc Natl Acad Sci USA 85:237–241PubMedCrossRef Hebbel RP, Morgan WT, Eaton JW, Hedlund BE (1988) Accelerated autoxidation and heme loss due to instability of sickle hemoglobin. Proc Natl Acad Sci USA 85:237–241PubMedCrossRef
46.
go back to reference Scott MD (2006) H2O2 injury in beta thalassemic erythrocytes: protective role of catalase and the prooxidant effects of GSH. Free Radic Biol Med 40:1264–1272PubMedCrossRef Scott MD (2006) H2O2 injury in beta thalassemic erythrocytes: protective role of catalase and the prooxidant effects of GSH. Free Radic Biol Med 40:1264–1272PubMedCrossRef
47.
go back to reference Cao GH, Prior RL (1998) Comparison of different analytical methods for assessing total antioxidant capacity of human serum. Clin Chem 44:1309–1315PubMed Cao GH, Prior RL (1998) Comparison of different analytical methods for assessing total antioxidant capacity of human serum. Clin Chem 44:1309–1315PubMed
48.
go back to reference Erel O (2004) A novel automated direct measurement method for total antioxidant capacity using a new generation, more stable ABTS radical cation. Clin Biochem 37:277–285PubMedCrossRef Erel O (2004) A novel automated direct measurement method for total antioxidant capacity using a new generation, more stable ABTS radical cation. Clin Biochem 37:277–285PubMedCrossRef
49.
go back to reference Fasola F, Adedapo K, Anetor J, Kuti M (2007) Total antioxidants status and some hematological values in sickle cell disease patients in steady state. J Natl Med Assoc 99:891–894PubMed Fasola F, Adedapo K, Anetor J, Kuti M (2007) Total antioxidants status and some hematological values in sickle cell disease patients in steady state. J Natl Med Assoc 99:891–894PubMed
50.
go back to reference Shimauti EL, Silva DG, de Almeida EA, Zamaro PJ, Belini Junior E, Bonini-Domingos CR (2010) Serum melatonin level and oxidative stress in sickle cell anemia. Blood Cells Mol Dis 45:297–301PubMedCrossRef Shimauti EL, Silva DG, de Almeida EA, Zamaro PJ, Belini Junior E, Bonini-Domingos CR (2010) Serum melatonin level and oxidative stress in sickle cell anemia. Blood Cells Mol Dis 45:297–301PubMedCrossRef
51.
go back to reference Silva DG, Belini Junior E, Torres LS, Ricci Junior O, Lobo CC, Bonini-Domingos CR et al (2011) Relationship between oxidative stress, glutathione S-transferase polymorphisms and hydroxyurea treatment in sickle cell anemia. Blood Cells Mol Dis 47:23–28PubMedCrossRef Silva DG, Belini Junior E, Torres LS, Ricci Junior O, Lobo CC, Bonini-Domingos CR et al (2011) Relationship between oxidative stress, glutathione S-transferase polymorphisms and hydroxyurea treatment in sickle cell anemia. Blood Cells Mol Dis 47:23–28PubMedCrossRef
52.
go back to reference Poillon WN, Kim BC, Rodgers GP, Noguchi CT, Schechter AN (1993) Sparing effect of hemoglobin-F and hemoglobin-A2 on the polymerization of hemoglobin-S at physiological ligand saturations. Proc Natl Acad Sci U S A 90:5039–5043PubMedCrossRef Poillon WN, Kim BC, Rodgers GP, Noguchi CT, Schechter AN (1993) Sparing effect of hemoglobin-F and hemoglobin-A2 on the polymerization of hemoglobin-S at physiological ligand saturations. Proc Natl Acad Sci U S A 90:5039–5043PubMedCrossRef
53.
go back to reference Dasgupta T, Fabry ME, Kaul DK (2010) Antisickling property of fetal hemoglobin enhances nitric oxide bioavailability and ameliorates organ oxidative stress in transgenic-knockout sickle mice. Am J Physiol Regul Integr Comp Physiol 298:R394–R402PubMedCrossRef Dasgupta T, Fabry ME, Kaul DK (2010) Antisickling property of fetal hemoglobin enhances nitric oxide bioavailability and ameliorates organ oxidative stress in transgenic-knockout sickle mice. Am J Physiol Regul Integr Comp Physiol 298:R394–R402PubMedCrossRef
54.
go back to reference Steinberg MH (2009) Genetic etiologies for phenotypic diversity in sickle cell anemia. Scientific World Journal 9:46–67PubMedCrossRef Steinberg MH (2009) Genetic etiologies for phenotypic diversity in sickle cell anemia. Scientific World Journal 9:46–67PubMedCrossRef
55.
go back to reference Agil A, Sadrzadeh SMH (2000) Hydroxy-urea protects erythrocytes against oxidative damage. Redox Rep 5:29–34PubMed Agil A, Sadrzadeh SMH (2000) Hydroxy-urea protects erythrocytes against oxidative damage. Redox Rep 5:29–34PubMed
56.
go back to reference Glickstein H, Ben El R, Link G, Breuer W, Konijn AM, Hershko C et al (2006) Action of chelators in iron-loaded cardiac cells: accessibility to intracellular labile iron and functional consequences. Blood 108:3195–3203PubMedCrossRef Glickstein H, Ben El R, Link G, Breuer W, Konijn AM, Hershko C et al (2006) Action of chelators in iron-loaded cardiac cells: accessibility to intracellular labile iron and functional consequences. Blood 108:3195–3203PubMedCrossRef
57.
go back to reference Wood JC, Tyszka JM, Carson S, Nelson MD, Coates TD (2004) Myocardial iron loading in transfusion-dependent thalassemia and sickle cell disease. Blood 103:1934–1936PubMedCrossRef Wood JC, Tyszka JM, Carson S, Nelson MD, Coates TD (2004) Myocardial iron loading in transfusion-dependent thalassemia and sickle cell disease. Blood 103:1934–1936PubMedCrossRef
58.
go back to reference Kaul DK, Liu XD, Choong S, Belcher JD, Vercellotti GM, Hebbel RP (2004) Anti-inflammatory therapy ameliorates leukocyte adhesion and microvascular flow abnormalities in transgenic sickle mice. Am J Physiol Heart Circ Physiol 287:H293–H301PubMedCrossRef Kaul DK, Liu XD, Choong S, Belcher JD, Vercellotti GM, Hebbel RP (2004) Anti-inflammatory therapy ameliorates leukocyte adhesion and microvascular flow abnormalities in transgenic sickle mice. Am J Physiol Heart Circ Physiol 287:H293–H301PubMedCrossRef
59.
go back to reference Sultana C, Shen YM, Rattan V, Johnson C, Kalra VK (1998) Interaction of sickle erythrocytes with endothelial cells in the presence of endothelial cell conditioned medium induces oxidant stress leading to transendothelial migration of monocytes. Blood 92:3924–3935PubMed Sultana C, Shen YM, Rattan V, Johnson C, Kalra VK (1998) Interaction of sickle erythrocytes with endothelial cells in the presence of endothelial cell conditioned medium induces oxidant stress leading to transendothelial migration of monocytes. Blood 92:3924–3935PubMed
60.
go back to reference Vichinsky EP, Ohene-Frempong K (2011) Approaches to transfusion therapy and iron overload in patients with sickle cell disease: results of an international survey. Pediatr Hematol Oncol 28:37–42PubMedCrossRef Vichinsky EP, Ohene-Frempong K (2011) Approaches to transfusion therapy and iron overload in patients with sickle cell disease: results of an international survey. Pediatr Hematol Oncol 28:37–42PubMedCrossRef
63.
go back to reference Droge W (2002) Free radicals in the physiological control of cell function. Physiol Rev 82:47–95PubMed Droge W (2002) Free radicals in the physiological control of cell function. Physiol Rev 82:47–95PubMed
64.
go back to reference Kolb AM, Smit NPM, Lentz-Ljuboje R, Osanto S, van Pelt J (2009) Non-transferrin bound iron measurement is influenced by chelator concentration. Anal Biochem 385:13–19PubMedCrossRef Kolb AM, Smit NPM, Lentz-Ljuboje R, Osanto S, van Pelt J (2009) Non-transferrin bound iron measurement is influenced by chelator concentration. Anal Biochem 385:13–19PubMedCrossRef
65.
go back to reference Koren A, Fink D, Admoni O, Tennenbaum-Rakover Y, Levin C (2010) Non-transferrin bound labile plasma iron and iron overload in sickle cell disease: a comparative study between sickle cell disease and beta thalassemic patients. Eur J Haematol 84:72–78PubMedCrossRef Koren A, Fink D, Admoni O, Tennenbaum-Rakover Y, Levin C (2010) Non-transferrin bound labile plasma iron and iron overload in sickle cell disease: a comparative study between sickle cell disease and beta thalassemic patients. Eur J Haematol 84:72–78PubMedCrossRef
Metadata
Title
Oxidative stress and antioxidant capacity in sickle cell anaemia patients receiving different treatments and medications for different periods of time
Authors
Edis Belini Junior
Danilo Grünig Humberto da Silva
Lidiane de Souza Torres
Eduardo Alves de Almeida
Rodolfo Delfini Cancado
Carlos Chiattone
Claudia Regina Bonini-Domingos
Publication date
01-04-2012
Publisher
Springer-Verlag
Published in
Annals of Hematology / Issue 4/2012
Print ISSN: 0939-5555
Electronic ISSN: 1432-0584
DOI
https://doi.org/10.1007/s00277-011-1340-y

Other articles of this Issue 4/2012

Annals of Hematology 4/2012 Go to the issue
Obesity Clinical Trial Summary

At a glance: The STEP trials

A round-up of the STEP phase 3 clinical trials evaluating semaglutide for weight loss in people with overweight or obesity.

Developed by: Springer Medicine

Highlights from the ACC 2024 Congress

Year in Review: Pediatric cardiology

Watch Dr. Anne Marie Valente present the last year's highlights in pediatric and congenital heart disease in the official ACC.24 Year in Review session.

Year in Review: Pulmonary vascular disease

The last year's highlights in pulmonary vascular disease are presented by Dr. Jane Leopold in this official video from ACC.24.

Year in Review: Valvular heart disease

Watch Prof. William Zoghbi present the last year's highlights in valvular heart disease from the official ACC.24 Year in Review session.

Year in Review: Heart failure and cardiomyopathies

Watch this official video from ACC.24. Dr. Biykem Bozkurt discuss last year's major advances in heart failure and cardiomyopathies.