Abstract
Sickling of erythrocytes from patients with sickle cell anemia can be completely inhibited by exposure to nitrogen mustard (HN 2). Reaction of hemoglobin (Hb) S with increasing quantities of HN 2 produces a progressive rise in the minimum concentration of hemoglobin required for gelation on deoxygenation. Quantities of HN 2 sufficient to alter gelation cause no observable change in oxygen affinity or in heme:heme interaction. Preliminary studies of osmotic fragility and autohemolysis showed no abnormalities after erythrocytes were treated with HN 2. Due to the known toxicity of HN 2, no “in vivo” intravenous therapy with this agent can be considered.
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