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Research Article Free access | 10.1172/JCI105520

Concomitant Alterations of Sodium Flux and Membrane Phospholipid Metabolism in Red Blood Cells: Studies in Hereditary Spherocytosis

Harry S. Jacob and Manfred L. Karnovsky

Thorndike Memorial Laboratory and Second and Fourth [Harvard] Medical Services, Boston City Hospital, Boston, Mass.

Department of Medicine, Harvard Medical School, Boston, Mass.

Department of Biological Chemistry, Harvard Medical School, Boston, Mass.

St. Elizabeth's Hospital and Tufts Medical School, Boston, Mass.

†

Address requests for reprints to Dr. Harry S. Jacob, St. Elizabeth's Hospital, 736 Cambridge St., Brighton, Mass.

*

Submitted for publication June 8, 1966; accepted October 20, 1966.

Supported in part by grants HE-07652, T1-AM-5391, HE-10053, and AI-03260 from the National Institutes of Health.

Find articles by Jacob, H. in: PubMed | Google Scholar

Thorndike Memorial Laboratory and Second and Fourth [Harvard] Medical Services, Boston City Hospital, Boston, Mass.

Department of Medicine, Harvard Medical School, Boston, Mass.

Department of Biological Chemistry, Harvard Medical School, Boston, Mass.

St. Elizabeth's Hospital and Tufts Medical School, Boston, Mass.

†

Address requests for reprints to Dr. Harry S. Jacob, St. Elizabeth's Hospital, 736 Cambridge St., Brighton, Mass.

*

Submitted for publication June 8, 1966; accepted October 20, 1966.

Supported in part by grants HE-07652, T1-AM-5391, HE-10053, and AI-03260 from the National Institutes of Health.

Find articles by Karnovsky, M. in: PubMed | Google Scholar

Published February 1, 1967 - More info

Published in Volume 46, Issue 2 on February 1, 1967
J Clin Invest. 1967;46(2):173–185. https://doi.org/10.1172/JCI105520.
© 1967 The American Society for Clinical Investigation
Published February 1, 1967 - Version history
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Abstract

The role of membrane phosphatides in transport processes has been investigated in red cells from splenectomized patients with hereditary spherocytosis (HS).

Incorporation of inorganic 32phosphate into the membrane phosphatides of HS red cells was approximately twice normal, coinciding with the nearly twofold increment in flux of sodium ions in the cells.

A consistent, inordinate increase in specific activity of a chromatographic fraction containing phosphatidylserine provided the bulk of the over-all increase in labeling of HS red cell phosphatides. The specific activity of phosphatidic acid was increased but not consistently.

Radioactivity of the “acidic phosphatides” (phosphatidylserine and phosphatidic acid fractions) decreased, in general, when the sodium flux was low, i.e., when the cells were suspended in media of low sodium content. When the cation flux was elevated (hypotonic media), there was a marked (ca. 35%) increase in the labeling of phosphatidylserine fractions. Normal red cells whose permeability to cations was increased by exposure to 0.5 N butanol also exhibited increased labeling of acidic phosphatides.

Considerations of the stoichiometry of cation transport and phosphatide labeling make it unlikely that phospholipids act directly as carrier molecules for cations in red cell membranes. On the other hand, the involvement of these lipid substances in cation movements is substantiated by correlating several different states of sodium flux with the labeling of the phosphatidic acid and phosphatidylserine fractions.

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