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 H 2O 2 treatment. However when H 2O 2 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.