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Hemolysis and deformability of erythrocytes exposed to butoxyacetic acid, a metabolite of 2‐Butoxyethanol: II. Resistance in red blood cells from humans with potential susceptibility
Author(s) -
Udden Mark M.
Publication year - 1994
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.2550140207
Subject(s) - hemolysis , red blood cell , hereditary spherocytosis , erythrocyte fragility , red cell , metabolite , erythrocyte deformability , hemolytic anemia , chemistry , biology , immunology , biochemistry , medicine
2‐Butoxyethanol causes hemolysis in rodents but not in humans. 2‐Butoxyethanol‐induced hemolysis is primarily due to the effect of its metabolite 2‐butoxyacetic acid (BAA). 2‐Butoxyacetic acid did not cause hemolytic effects when incubated with blood from a limited number of normal individuals. Because 2‐butoxyethanol is contained in many consumer products, the possibility that there may be human subpopulations susceptible to hemolysis by BAA was examined. 2‐Butoxyacetic acid was incubated with red blood cells from healthy young and older individuals and with red blood cells from patients with hereditary spherocytosis and sickle cell disease. After incubation of red blood cells with or without 2.0 mM BAA for up to 4 h, conditions that readily hemolyzed rat red blood cells, there was no increase in hemolysis or changes in mean cellular volume or morphology. The deformability of erythrocytes treated with BAA was also measured using a nuclepore filtration technique. No changes in deformability due to treatment with BAA were detected. Although BAA is a potent cause of hemolysis in rats, red blood cells in humans, including the elderly and patients with two disorders marked by chronic hemolysis, were not susceptible to BAA‐induced hemolysis or loss of deformability.