Hydroxyurea has the capacity to induce damage to human erythrocytes which can be modified by radical scavengers.
The treatment of human erythrocytes with hydroxyurea [HU] results in the azide-dependent changes in osmotic fragility and in increased methemoglobin formation. Similar changes were induced by H2O2 treatment. However when H2O2 in the presence of azide stimulated malondialdehyde production, in the HU-treated cells no malondialdehyde was detectable. When subjected to an oxidant stress [sodium ascorbate] HU-treated erythrocytes were more fragile and revealed changes in the absorption spectrum of the TBA-reactive material in comparison with the cells treated with ascorbate alone. Partial protection by radical scavengers against certain HU-induced changes can be achieved. The results indicate that HU can damage erythrocytes and suggest the radical origin of these effects.
D001205:Ascorbic Acid / Q000494:pharmacology; D004912:Erythrocytes / Q000187:drug effects* / Q000502:physiology; D005609:Free Radicals; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology; D006918:Hydroxyurea / Q000494:pharmacology*; D008054:Lipid Peroxides / Q000097:blood; D008706:Methemoglobin / Q000378:metabolism; D009996:Osmotic Fragility / Q000187:drug effects; D014810:Vitamin E / Q000494:pharmacology
D005609:Free Radicals; D008054:Lipid Peroxides; D014810:Vitamin E; D008706:Methemoglobin; D006861:Hydrogen Peroxide; D001205:Ascorbic Acid; D006918:Hydroxyurea