Erythrocyte Energy Metabolism in Hereditary Spherocytosis

Claude F. Reed; Lawrence E. Young

doi:10.1172/JCI105613

Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, N. Y.

†

Address requests for reprints to Dr. Lawrence E. Young, The University of Rochester School of Medicine and Dentistry, Rochester, N. Y. 14620.

Submitted for publication May 18, 1966; accepted April 6, 1967.

This investigation was supported by the U. S. Army Medical Research and Development Command, Department of the Army, under research contract DA-49-193-MD-2656, and by a Public Health Service Research Development Award (HE-6234) from the Heart Institute (Dr. Reed).

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Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, N. Y.

†

Address requests for reprints to Dr. Lawrence E. Young, The University of Rochester School of Medicine and Dentistry, Rochester, N. Y. 14620.

Submitted for publication May 18, 1966; accepted April 6, 1967.

Find articles by Young, L. in: PubMed | Google Scholar

Published July 1, 1967 - More info

Published in Volume 46, Issue 7 on July 1, 1967
J Clin Invest. 1967;46(7):1196–1204. https://doi.org/10.1172/JCI105613.
© 1967 The American Society for Clinical Investigation

Published July 1, 1967 - Version history

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Abstract

The incorporation of extracellular orthophosphate-³²P into cellular ATP, 2,3-diphosphoglyceric acid, and inorganic phosphate has been measured over a period of 6 hours in vitro in red blood cells from normal subjects and from patients with hereditary spherocytosis who had undergone splenectomy. The pattern of labeling of the intracellular compounds was found to be the same in both types of red blood cells, as reported by other workers using much shorter periods of incubation. In addition, in the present study it was possible to compare the net flux of extracellular phosphate into ATP between the two groups of erythrocytes. These latter results suggest that the actual turnover rate of ATP was not abnormal in these patients with hereditary spherocytosis.