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Research Article Free access | 10.1172/JCI106895

Potassium permeability in β-thalassemia minor red blood cells

Robert B. Gunn, David N. Silvers, and Wendell F. Rosse

Department of Physiology and Pharmacology, Duke University Medical Center, Durham, North Carolina 27710

Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710

Find articles by Gunn, R. in: PubMed | Google Scholar

Department of Physiology and Pharmacology, Duke University Medical Center, Durham, North Carolina 27710

Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710

Find articles by Silvers, D. in: PubMed | Google Scholar

Department of Physiology and Pharmacology, Duke University Medical Center, Durham, North Carolina 27710

Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710

Find articles by Rosse, W. in: PubMed | Google Scholar

Published May 1, 1972 - More info

Published in Volume 51, Issue 5 on May 1, 1972
J Clin Invest. 1972;51(5):1043–1050. https://doi.org/10.1172/JCI106895.
© 1972 The American Society for Clinical Investigation
Published May 1, 1972 - Version history
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Abstract

The intracellular content of K+ in thalassemia minor red blood cells is markedly reduced after incubation in autologous serum for 24 hr at 37°C. There is no compensatory increase in intracellular Na+ concentration of the cell thus reduced. This change is due to an acquired increase in selective permeability of the membrane to K+. This phenomenon follows the depletion of energy sources in the thalassemia minor cells but does not follow comparable depletion in normal cells. The loss of osmotically active intracellular contents probably accounts for the increased resistance of incubated thalassemia minor red blood cells to osmotic lysis.

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