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SL Schrier, I Junga and L Ma
When amphipathic cationic drugs are added to intact human RBCs, the RBCs
first undergo a stomatocytic shape change and then, if relatively large
amounts of drug are added and if the metabolic state of the RBC is
appropriate, endocytic vacuoles form. Vanadate has a structural similarity
to the transition state of phosphate, which presumably accounts for its
ability to inhibit phosphohydrolases, although other actions of vanadate
have been described. Vanadate inhibited three forms of drug-induced
endocytosis in intact RBCs despite the fact that the three drugs chosen
(primaquine, chlorpromazine, and vinblastine) are known to have differing
requirements for RBC ATP. Vanadate also inhibited the stomatocytic shape
change produced by primaquine, chlorpromazine, and vinblastine, but not the
stomatocytosis produced by low pH. Vanadate had no effect on RBC
echinocytosis produced by lysophosphatidylcholine. In studying endocytosis
in hypotonic, leaky, "white" ghosts, we discovered that vanadate inhibited
only the endocytosis produced by Mg-ATP and not the endocytosis produced by
manipulations that directly attack the cytoskeletal proteins. These
findings suggest that ATP hydrolysis has a role in some forms of
amphipathic cation-induced stomatocytosis and endocytosis in intact RBCs.
In addition, studies in ghosts support the idea that Mg-ATP does indeed
produce "energized" endocytosis dependent on utilization or hydrolysis of
ATP.
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| Copyright © 1986 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
