Glutathione Peroxidase Activity in Whole Blood of Patients with Sickle Cell Anaemia

Zimmerman, Carola Ponzetto; Natta, Clayton

doi:10.1111/j.1600-0609.1981.tb01644.x

Cited by 9 publications

(1 citation statement)

References 11 publications

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“…In the largest study, Chiu et al observed a significantly lower plasma vitamin E level (0.61 mg/dl) in 54 children and young adults with sickle cell disease than did 16 normal control subjects (0.89 mg/dl). It is of interest that sickle red cells have what may be compensatory increases in the activities of glutathione peroxidase [78,79] and superoxide dismutase [80]. It is of interest that sickle red cells have what may be compensatory increases in the activities of glutathione peroxidase [78,79] and superoxide dismutase [80].…”

Section: Fat Soluble Vitaminsmentioning

confidence: 99%

Nutrition and sickle cell disease

Reid

2012

Comptes Rendus. Biologies

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Section: Fat Soluble Vitaminsmentioning

confidence: 99%

Nutrition and sickle cell disease

Reid

2012

Comptes Rendus. Biologies

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Interaction between oxidized hemoglobin and the cell membrane: A common basis for severalfalciparum malaria-linked genetic traits

Destro‐Bisol¹,

Giardina²,

Sansonetti³

et al. 1996

Am. J. Phys. Anthropol.

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This paper focuses on the interaction between oxidized hemoglobin and the erythrocyte membrane, and its relevance to some falciparum malaria‐linked genetic traits. We first present the experimental evidence which suggests that the interaction between hemoglobin derivatives and membrane proteins is an important cellular mechanism for the erythrocytes carrying HbS, HbE, HbF, α‐ and β‐thalassemia, and G6PD deficiency. Thereafter, we show how the Hb/membrane interaction might act as primum movens for diverse cellular mechanisms which 1) reduce invasion of erythrocytes by the falciparum parasite; 2) impair parasite survival and development within the cell; 3) accelerate infected erythrocyte clearance by phagocytosis. We claim that oxidative stress is the driving force of this process, since highly reactive species (like O2− and H2O2) mediate the gradual oxidation of Hb to irreversible hemichrome‐containing Heinz bodies. We therefore suggest that positing the interaction between oxidized hemoglobin and cell membrane as a common basis for several falciparum malaria‐linked genetic traits is not only consistent with experimental evidence gathered so far, but provides a new, clearer perspective: the molecular event on which these known protective traits rest. In the last part of the paper we will discuss two case studies which provide further support for the role played by hemoglobin derivatives and membrane proteins: 1) the influence of a cyanogen‐rich diet on the distribution of Hbβ*S gene frequencies in Liberia (Jackson [1990] Am. J. Hum. Biol. 2:521–532); and 2) population data on polymorphisms at the Hbβ and GPXI loci (Destro‐Bisol and Spedini [1989] Am. J. Phys. Anthropol. 79:217–224). © 1996 Wiley‐Liss, Inc.

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Impaired pentose phosphate shunt function in sickle cell disease: A potential mechanism for increased heinz body formation and membrane lipid peroxidation

1983

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The red cells' antioxidant defense mechanisms were compared between individuals with sickle cell disease and those with hemolytic anemia and reticulocytosis. In sickle cell disease, there was a significant increase in incubated Heinz body formation (p less than .001), a decrease in reduced glutathione concentration (p less than .01), an increase in glucose-6-phosphate dehydrogenase activity (p less than .01), and a decrease in glutathione reductase activity (p less than .005). The patients with sickle cell disease hd an absolute increase in the activity of the pentose shunt in the intact red cell after methylene blue stimulation (p less than .05) and in red cell hemolysates (p less than .0250. Heinz body formation (r = .75) and pentose shunt activity in red cell hemolysates (r = .83) were strongly related to the degree of reticulocytosis. Although there was a correlation between the pentose shunt activity in the stimulated red cell and in red cell hemolysates for the patients with hemolytic anemia (r = .58), stimulated shunt activity did not increase as the hemolysate shunt activity increased for the patients with sickle cell disease. There were very strong relationships between the ATP concentration and the reticulocyte count (r = .80) and the hemolysate pentose shunt activity (r = .77) in sickle cel disease. These data suggest that in spite of an absolute increase in stimulated pentose shunt activity, there Is a relative suppression of stimulated shunt activity in the youngest sickle erythrocytes. This may be related, in part, to the inhibitory effects of high concentrations of ATP on the activity of glucose-6-phosphate dehydrogenase.

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Glutathione Peroxidase Activity in Whole Blood of Patients with Sickle Cell Anaemia

Cited by 9 publications

References 11 publications

Nutrition and sickle cell disease

Nutrition and sickle cell disease

Interaction between oxidized hemoglobin and the cell membrane: A common basis for severalfalciparum malaria-linked genetic traits

Impaired pentose phosphate shunt function in sickle cell disease: A potential mechanism for increased heinz body formation and membrane lipid peroxidation

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