A sodium-specific membrane permeability defect induced by phospholipid vesicle treatment of erythrocytes.
Treatment of human erythrocytes with phospholipid vesicles induces a selective membrane permeability defect which leads to osmotic lysis. The defective cells exhibit a massive sodium ion leak while maintaining normal impermeability to other cations, anions, and neutral small molecules. The sodium ion influx and resulting hemolysis may be inhibited by increased pH, by tetrodotoxin, and by reintroduction of vesicle-extracted proteins into the cell. These characteristics suggest that phospholipid vesicle treatment destroys the cell by disrupting a membrane protein system involved in regulation of cation permeability.
D000251:Adenosine Triphosphatases / Q000097:blood; D000328:Adult; D002463:Cell Membrane Permeability / Q000187:drug effects*; D004910:Erythrocyte Membrane / Q000187:drug effects*; D004912:Erythrocytes / Q000187:drug effects*; D006461:Hemolysis; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008565:Membrane Proteins / Q000378:metabolism; D008567:Membranes, Artificial; D010713:Phosphatidylcholines / Q000494:pharmacology*; D012964:Sodium / Q000378:metabolism*; D013779:Tetrodotoxin / Q000494:pharmacology
D008565:Membrane Proteins; D008567:Membranes, Artificial; D010713:Phosphatidylcholines; D013779:Tetrodotoxin; D012964:Sodium; D000251:Adenosine Triphosphatases