Hemoglobin S-mediated membrane oxidant injury: protection from malaria and pathology in sickle cell disease.
It is suggested here that a Hemoglobin S (HbS)-mediated membrane oxidant injury is responsible for both the protection from malaria infection in the heterozygous sickle cell state, and for a critical pathologic process in homozygous sickle cell disease. This suggestion is arrived at by applying to the HbS condition the oxidant stress model for malaria resistance. Such a model had been developed to explain the protection from malaria in thalassemia and in glucose-6-phosphate dehydrogenase (G6PD) deficiency (9).
D000755:Anemia, Sickle Cell / Q000473:pathology*; D004910:Erythrocyte Membrane / Q000378:metabolism; D004912:Erythrocytes / Q000469:parasitology; D005955:Glucosephosphate Dehydrogenase Deficiency / Q000378:metabolism; D006450:Hemoglobin SC Disease / Q000378:metabolism / Q000473:pathology*; D006454:Hemoglobins / Q000378:metabolism*; D006579:Heterozygote; D006801:Humans; D008288:Malaria / Q000517:prevention & control*; D008954:Models, Biological; D010084:Oxidation-Reduction; D013789:Thalassemia / Q000378:metabolism
D006454:Hemoglobins