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The shedding of acetylcholinesterase-enriched vesicles from erythrocytes of various species of animals occurred when cells were treated with C12:0PC. The response was observed shortly after a morphological change of erythrocytes without any accompanying detectable K+ leakage or hemolysis. The vesiculation was inhibited by the presence of serum albumin or by the incorporation of cholesterol into C12:0PC liposomes, indicating that the insertion of C12:0PC into the erythrocyte membrane causes the vesiculation. The ratio of C12:0PC to total phospholipid determined in vesicle fractions was almost the same as that observed in non-hemolyzed cell fractions. This finding suggests that the vesicles were not shed from portions of membranes rich in C12:0PC. The vesicles showed similar characteristics to those generated by ATP depletion; their diameter is 150-200 nm and they are enriched with acetylcholinesterase activity. Erythrocytes became denser when they lost acetylcholinesterase activity on treatment with C12:0PC.
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