Oxidant damage of normal and glucose 6-phosphate dehydrogenase (G6PD)-deficient red blood cells is enhanced by iron-EDTA complex.
A combination of divicine (an aglycone from the fava bean beta-glucoside vicine) and ascorbate results in a marked production of ethylene from methional, as a probable indication of OH radical formation. Addition of iron-EDTA to this oxidising system enhances the ethylene production significantly. The enhancing effect of iron-EDTA is also observed when both normal and Glucose 6-phosphate dehydrogenase (G6PD)-deficient red cells are exposed to the divicine-ascorbate system. Moreover, iron-EDTA magnifies other consequences of oxidant damage afforded by divicine-ascorbate or by ascorbate alone on the target red cells, such as depletion of reduced glutathione, formation of methemoglobin, stimulation of hexose monophosphate shunt activity and lipid peroxidation. Although the biochemical changes induced by this oxidative system are not remarkably different in normal and in G6PD-deficient red cells, the extra-damaging effect of chelated iron might be important in the mechanism of hemolysis.
D001205:Ascorbic Acid / Q000494:pharmacology*; D002374:Catalase / Q000378:metabolism; D004492:Edetic Acid / Q000494:pharmacology*; D004912:Erythrocytes / Q000187:drug effects / Q000502:physiology*; D005290:Ferric Compounds / Q000494:pharmacology*; D005609:Free Radicals; D005955:Glucosephosphate Dehydrogenase Deficiency / Q000097:blood*; D005978:Glutathione / Q000097:blood; D006801:Humans; D006878:Hydroxides / Q000097:blood; D017665:Hydroxyl Radical; D007501:Iron / Q000494:pharmacology*; D008297:Male; D010100:Oxygen / Q000097:blood; D011744:Pyrimidinones / Q000494:pharmacology*
D005290:Ferric Compounds; D005609:Free Radicals; D006878:Hydroxides; D011744:Pyrimidinones; C026511:divicine; D017665:Hydroxyl Radical; D004492:Edetic Acid; D007501:Iron; D002374:Catalase; D005978:Glutathione; C019179:Fe(III)-EDTA; D001205:Ascorbic Acid; D010100:Oxygen