Aspirin-induced hemolysis: the role of concomitant oxidant (H2O2) challenge.
Studies were conducted in an attempt to determine the hemolytic potential of acetylsalicylic acid (ASA) on normal intact red blood cells (RBCs). ASA (25 mg/100 ml) did not impair RBC G-6-PD, glutathione peroxidase or catalase activity, glutathione stability, or hexose monophosphate shunt activity. Hemolysis was not observed after incubation with ASA alone but was quickly noted after exposure to ASA (25 mg/100 ml) and H2O2 (1.2%). Hemolysis did not occur with H2O2 alone but was directly proportional to the ASA concentration. Hemolysis was preceded by peroxidation of membrane lipid and was inhibited by the presence of the antioxidant, thymol. With ASA and H2O2 a marked reduction in membrane phosphatidyl ethanolamine occurred with oxidation of 20:4 and 22:6 fatty acids. No effect on phospholipids or fatty acids occurred with either ASA or H2O2 alone. Salicylic acid, singly or with H2O2, does not exhibit these effects.
D000328:Adult; D001241:Aspirin / Q000494:pharmacology*; D004910:Erythrocyte Membrane / Q000187:drug effects; D004912:Erythrocytes / Q000187:drug effects*; D005841:Gentisates / Q000494:pharmacology; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006461:Hemolysis / Q000187:drug effects*; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology*; D066298:In Vitro Techniques; D008563:Membrane Lipids / Q000378:metabolism
D005841:Gentisates; D008563:Membrane Lipids; D006861:Hydrogen Peroxide; D005954:Glucosephosphate Dehydrogenase; D005979:Glutathione Peroxidase; D001241:Aspirin