Peroxidation, Vitamin E, and Sickle‐cell Anemia*

Abstract

In summary, we propose the following scheme (Figure 5) to describe the role of peroxidation in the pathophysiology of SCA. Sickle erythrocytes are more susceptible to peroxidation than are normal erythrocytes. This increased susceptibility to peroxidation is, in part, due to decreased blood vitamin E levels and abnormal membrane phospholipid organization induced by sickling. The peroxidative damage of sickle erythrocytes may accelerate or contribute to loss of cell deformability and to chronic hemolysis. Peroxidative damage can produce abnormal cellular properties, such as potassium leak and reduced filterability, and contribute to formation of ISCs. Increased red cell rigidity can initiate episodes of capillary obstruction, leading to vasoocclusive painful crises and to tissue infarction. Liver dysfunction as well as increased production of bilirubin secondary to hemolysis could result in bile sludging and decreased secretion of bile salts into the intestinal lumen. Reduced bile salt secretion leads to partial fat and vitamin E malabsorption. Vitamin E deficiency enhances red cell susceptibility to peroxidation and promotes a vicious cycle in SCA. Although we have not studied factors that might initiate peroxidative damage, sickle hemoglobin and excess body iron should be considered as potential sources. Our studies suggest that vitamin E supplementation to sickle-cell patients could be of clinical benefit.

Nutrition and sickle cell disease

“…A similar study by Chiu et a1 found no significant change in ISCs despite an increase in vitamin E [92]. One difference between the two studies was that Natta's population had a pretreatment ISC count of 25 % [93] while in Chiu's study the pretreatment ISC count was only 12 % [92]. Also confounding any possible therapeutic response to vitamin E is the well recognized difficulty of accurately and reproducibly counting ISCs [94].…”

Selenium and Glutathione Peroxidase Levels in Sickle Cell Anemia

“…While diets in North America generally provide adequate amounts of Se [4], there is no information available concerning the Se of SCA patients. Studies from several laborato ries have suggested that in SCA there is an increased production of free radicals in the body [7][8][9], Levels of vitamin E, an antioxidant micronutrient, in patients with SCA have been reported to be lower than in nor mal subjects [5,6]. In this study we report the data on Se and glutathione peroxidase in both plasma and whole blood of SCA patients and controls.…”

“…In addition to Se and glutathione peroxi dase, however, the levels of such important antioxi dant systems as vitamin E [5,6], vitamin C [17] and carotenoids [18] have been reported to be lower in SCA patients than normal controls. Zinc levels have also been reported to be lower in SCA patients [19].…”

Cellular Immunity to Malaria and Babesia Parasites: A Personal Viewpoint

“…However, Roth et al (1983) have shown that P. falciparum grows poorly in ery-throcytes from persons hemizygous or heterozygous for the Mediterranean variety of G6PD deficiency even in the presence of 17% O2 ; presumably the protection would be even greater under conditions of oxidant stress. Since there is good evidence that erythrocytes containing HbS are sensitive to oxidant stress (Chiu et al, 1982), replication of P. falciparum may also be inhibited in these cells under such conditions. P. falciparum grows poorly in erythrocytes containing HbC or HbE .…”