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Hemolytic properties of human erythrocytes in hereditary spherocytosis (HS) were examined under hydrostatic pressure or hypotonic conditions. In the hypotonic buffer, HS erythrocytes were more fragile than normal erythrocytes, and the osmotic fragility was similarly enhanced if both erythrocytes were treated with 4,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS), an anion transport inhibitor. On the other hand, the hemolysis of HS erythrocytes at 200 MPa was almost the same degree as that of normal cells. Upon DIDS treatment, the hemolysis of normal erythrocytes at 200 MPa was suppressed by about 35%, whereas that of HS erythrocytes was not affected. The absence of a suppressive effect of DIDS on high-pressure-induced hemolysis is likely to be HS-specific and may be a reflection of the underlying defects of band 3-cytoskeleton interactions in HS erythrocytes.

High-Pressure-lnduced Hemolysis of Hereditary Spherocytic Erythrocytes Is Not Suppressed by DIDS Labeling.