Incubation of human red blood cells with 0.01 and 0.02 m monomethylhydrazine (MMH) denatures hemoglobin and precipitates it both diffusely throughout the cytoplasmic compartment and in a concentrated form as Heinz bodies. Concomitantly, there is a decrease in red cell deformability (filterability), when measured as a function of the time required for passage of red cells through Millipore filters. Acetylphenylhydrazine (APH) produces Heinz bodies that attach to the cell membrane and distort the cell membrane, and also alters red cell deformability. These alterations in deformability in APH-injured cells have been attributed to Heinz body-cell membrane interactions. Unlike APH-induced Heinz bodies, MMH-induced Heinz bodies show little affinity for the cell membrane and are free of the membrane when decreases in deformability are first detected. These results show that alterations in red cell deformability with oxidative injury may be unrelated to Heinz body-cell membrane interactions. Ultrastructural observations suggest that denatured hemoglobin diffusely distributed in the cytoplasm may polymerize into a loose network and account for the altered rheological properties of MMH-injured red cells.
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