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Red Blood Cell Membrane Storage Lesion
Author(s) -
Schrier S. L.,
Hardy B.,
Bensch K.,
Junga I.,
Krueger J.
Publication year - 1979
Publication title -
transfusion
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.045
H-Index - 132
eISSN - 1537-2995
pISSN - 0041-1132
DOI - 10.1046/j.1537-2995.1979.19279160285.x
Subject(s) - endocytosis , primaquine , microbiology and biotechnology , receptor mediated endocytosis , cell membrane , lesion , membrane , biology , chemistry , biochemistry , cell , immunology , medicine , chloroquine , pathology , malaria
Storage of human erythrocytes in CPO produced a lesion of the erythrocyte membrane manifested by abnormal endocytosis in resealed ghosts and in intact erythrocytes. Endocytosis produced by resealing Ca, Mg, and ATP into ghosts was impaired by five weeks of storage and this defect was promptly reversed by the prior regeneration of ATP in the stored erythrocytes. Drug‐induced endocytosis was studied in intact stored erythrocytes. Vinblastine endocytosis was not affected by storage. Chlorpromazine endocytosis was variably but never completely inhibited by storage, and restoration of ATP occasionally resulted in complete restoration of chlorpromazine endocytosis to base line values. However, primaquine endocytosis was usually totally inhibited after three to four weeks of storage at a time when residual ATP levels were 30 to 50 per cent of base line values. Restoration of ATP levels to at least base line values did not completely restore primaquine endocytosis to control values. Study of primaquine endocytosis provides an opportunity for defining an erythrocyte membrane storage lesion.