Oxidative process in erythrocytes of individuals with hemoglobin S

Chaves, Michele Ana Flores; Leonart, Maria Suely Soares; Nascimento, Aguinaldo José do

doi:10.1179/102453308x343356

Cited by 37 publications

(32 citation statements)

References 21 publications

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“…Sickle cell erythrocytes generate approximately twofold higher quantities of reactive oxygen species due to the instability of HbS26. As a consequence, the levels of methaemoglobin and irreversibly oxidized haemichromes are significantly elevated in HbAS erythrocytes relative to wild-type erythrocytes29, as verified in our study by Mössbauer spectroscopy ( P <0.01 according to Kruskal–Wallis one-way analysis of variance test; Table 1). Similarly, elevated levels of methaemoglobin and irreversibly oxidized haemichromes were observed in HbAC and HbF erythrocytes (Table 1)3.…”

Section: Resultssupporting

confidence: 81%

“…Our finding that a transient oxidative insult before infection can induce comparable phenotypes in parasitized HbAA erythrocytes points towards intracellular oxidative stress as the common underlying principle. This conclusion is further supported by the oxidative imbalance inherent to haemoglobinopathic and fetal erythrocytes (Table 1)324262729.…”

Section: Discussionmentioning

confidence: 72%

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Oxidative insult can induce malaria-protective trait of sickle and fetal erythrocytes

et al. 2016

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Plasmodium falciparum infections can cause severe malaria, but not every infected person develops life-threatening complications. In particular, carriers of the structural haemoglobinopathies S and C and infants are protected from severe disease. Protection is associated with impaired parasite-induced host actin reorganization, required for vesicular trafficking of parasite-encoded adhesins, and reduced cytoadherence of parasitized erythrocytes in the microvasculature. Here we show that aberrant host actin remodelling and the ensuing reduced cytoadherence result from a redox imbalance inherent to haemoglobinopathic and fetal erythrocytes. We further show that a transient oxidative insult to wild-type erythrocytes before infection with P. falciparum induces the phenotypic features associated with the protective trait of haemoglobinopathic and fetal erythrocytes. Moreover, pretreatment of mice with the pro-oxidative nutritional supplement menadione mitigate the development of experimental cerebral malaria. Our results identify redox imbalance as a causative principle of protection from severe malaria, which might inspire host-directed intervention strategies.

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Section: Resultssupporting

confidence: 81%

Section: Discussionmentioning

confidence: 72%

Oxidative insult can induce malaria-protective trait of sickle and fetal erythrocytes

et al. 2016

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“…Moreover, in SCD red blood cells are more susceptible to oxidation (Chaves, Leonart, Nascimento, 2008) and have a reduced ability to defend against oxidation (Fasola et al, 2007). The imbalance between pro-and antioxidant actions can lead to extensive oxidative damage of erythrocyte membrane components (Titus et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Ginkgo biloba extract (EGb 761) attenuates oxidative stress induction in erythrocytes of sickle cell disease patients

Furman

Henneberg

Hermann

et al. 2012

Braz. J. Pharm. Sci.

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Sickle cell disease promotes hemolytic anemia and occlusion of small blood vessels due to the presence of high concentrations of hemoglobin S, resulting in increased production of reactive oxygen species and decreased antioxidant defense capacity. The aim of this study was to evaluate the protective action of a standardized extract of Ginkgo biloba (EGb 761), selected due to its high content of flavonoids and terpenoids, in erythrocytes of patients with sickle cell anemia (HbSS, SS erythrocytes) subjected to oxidative stress using tert-butylhydroperoxide or 2,2-azobis-(amidinepropane)-dihydrochloride, in vitro. Hemolysis indexes, reduced glutathione, methemoglobin concentrations, lipid peroxidation, and intracellular reactive oxygen species were determined. SS erythrocytes displayed increased rates of oxidation of hemoglobin and membrane lipid peroxidation compared to normal erythrocytes (HbAA, AA erythrocytes), and the concentration of EGb 761 necessary to achieve the same antioxidant effect in SS erythrocytes was at least two times higher than in normal ones, inhibiting the formation of intracellular reactive oxygen species (IC50 of 13.6 µg/mL), partially preventing lipid peroxidation (IC50 of 242.5 µg/mL) and preventing hemolysis (IC50 of 10.5 µg/mL). Thus, EGb 761 has a beneficial effect on the oxidative status of SS erythrocytes. Moreover, EGb 761 failed to prevent oxidation of hemoglobin and reduced glutathione at the concentrations examined.

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“…6 The pro-oxidative action of tert-butyl hydroperoxide (TBHP) has been used to analyze the oxidative stress in isolated erythrocytes. 7 It can cause metabolic alterations such as unbalance on the homeostasis of intracellular calcium; oxidation of the reduced glutathione, and of proteins tiol groups; damages on DNA molecules; lipid peroxidation; lowering of the intracellular mobility of the membrane proteins. 8 The understanding of the oxidative stress mechanisms helps to explain many of the processes of cellular lesion and death, especially those related to the hemolytic diseases.…”

Section: Introductionmentioning

confidence: 99%

“…The oxidative action induced by TBHP was observed in erythrocytes from patients with sickle cell anemia by the increase on the content of Heinz bodies, methemoglobin, hemolysis, GSH depletion and lowering activities of the enzymes G6-PD and glutathione reductase (GR). 7 The aim of this work was the study on the effect of DFO and DFP in isolated erythrocytes from normal individuals and patients with β-thalassemias, under the prooxidative action of TBHP.…”

Section: Introductionmentioning

confidence: 99%

Protective action of deferiprone and deferoxamine in erythrocytes isolated from patients with β-thalassemias

Santos¹,

Baldanzi²,

Leonart³

et al. 2009

Rev. Bras. Hematol. Hemoter.

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One of the most deleterious consequences of iron overload in thalassemia is the presence of non-transferrin bound iron (NTBI), a free radical that acts as a catalyst for free oxygen radicals, in particular for hydroxyl free radicals (OH.). These radicals oxidize both membrane lipids and proteins causing irreversible damage to biologically important molecules and cellular structures. Treatment with iron chelators has been important to improve survival of these individuals. The aim of this work was the study on the effects of deferoxamine (DFO) and deferiprone (DFP) on erythrocytes under the pro-oxidative action of TBHP isolated from normal individuals and patients with ß-thalassemia. The in vitro action of deferoxamine and deferiprone on the oxidative metabolism of erythrocytes from ß-thalassemic patients treated at the Centro de Hematologia e Hemoterapia do Paraná (HEMEPAR), Brazil, under the pro-oxidative action of TBHP was studied. Methemoglobin concentrations, reduced glutathione (GSH), hemolysis indexes and the enzyme activities of G6-PD and GR were determined. The oxidation indexes were higher in erythrocytes of ß-thalassemic individuals than those from normal individuals. Treatment of the normal and ß-thalassemic erythrocytes with DFO and/or DFP protected against the formation of GSH promoted by TBHP. Rev. Bras. Hematol. Hemoter.

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Oxidative process in erythrocytes of individuals with hemoglobin S

Cited by 37 publications

References 21 publications

Oxidative insult can induce malaria-protective trait of sickle and fetal erythrocytes

Oxidative insult can induce malaria-protective trait of sickle and fetal erythrocytes

Ginkgo biloba extract (EGb 761) attenuates oxidative stress induction in erythrocytes of sickle cell disease patients

Protective action of deferiprone and deferoxamine in erythrocytes isolated from patients with β-thalassemias

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