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Storage of human erythrocytes causes membrane damage, impairing endocytosis. Primaquine-induced endocytosis is particularly sensitive to storage, offering a way to define this erythrocyte membrane storage lesion.
Area of Science:
- Blood banking
- Cell biology
- Membrane transport
Background:
- Erythrocyte storage in citrate-phosphate-dextrose (CPD) can lead to membrane lesions.
- Endocytosis, a crucial cellular process, may be affected by erythrocyte storage.
Purpose of the Study:
- To investigate the impact of erythrocyte storage on membrane integrity and endocytic function.
- To identify specific endocytic pathways sensitive to storage-induced lesions and ATP depletion.
Main Methods:
- Assessed endocytosis in resealed erythrocyte ghosts and intact stored erythrocytes.
- Utilized various drugs (vinblastine, chlorpromazine, primaquine) to induce endocytosis.
- Measured ATP levels and evaluated the effect of ATP regeneration on endocytic function.
Main Results:
- Storage impaired Ca, Mg, and ATP-induced endocytosis in ghosts, reversible by ATP regeneration.
- Vinblastine and chlorpromazine endocytosis were largely unaffected or variably inhibited by storage.
- Primaquine endocytosis was significantly inhibited after 3-4 weeks of storage, even with ATP restoration, indicating a specific storage lesion.
Conclusions:
- Erythrocyte storage in CPD induces a membrane lesion affecting endocytosis.
- Primaquine-induced endocytosis serves as a sensitive marker for defining and studying erythrocyte membrane storage lesions.
- Understanding these lesions is crucial for optimizing erythrocyte preservation and transfusion efficacy.
Abstract:
Storage of human erythrocytes in CPD 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 not affected by storage. Chlorpromazine endocytosis was variably but never completely inhibited 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 primaquine endocytosis to control values. Study of primaquine endocytosis provides an opportunity for defining an erythrocyte membrane storage lesion.