Glutathione Instability in Normal Blood
نویسنده
چکیده
T HE DEMONSTRATION of abnormality of red-cell glutathione metabolism in vitro in cases of primaquine induced hemolytic anemia1 and the observations of its correlation with red cell aging2 have stimulated investigations into mechanisms of hemolysis and normal red cell aging. Current knowledge suggests that this drug-induced hemolysis is closely related to a deficiency of erythrocyte glucose-6-phosphate dehydrogenase with its consequent metabolic defects.3 In the glutathione stability test, incubation of red cells from primaquine sensitive patients with appropriate drugs causes a drop in the level of reduced glutathione ( GSH ) . This is probably the result of an madequate supply of reduced triphosphopyridine nucleotide (TPNH ), normally provided by the action of glucose-6-phosphate dehydrogenase, which is required by glutathione reductase to maintain glutathione in a reduced states Since this phenomenon of hemolysis in vivo in the presence of one of these oxidant drugs has been demonstrated in a non-sensitive patient,5 erythrocyte glutathione stability was studied under varying circumstances to determine whether normal red cells might be made to appear “sensitive” in the in vitro tests.
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