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MR Clark and ME Rossi
Department of Laboratory Medicine, University of California, San Francisco
94143.
This study investigated the effect of acute deoxygenation on membrane
permeability characteristics of sickle cells. Measured fluxes of Na+ and K+
in ouabain-inhibited cells, of chloride and sulfate exchange in
4,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS)-inhibited and untreated
cells, and of erythritol, mannitol, and arabinose in cytochalasin
B-inhibited cells indicated that a deoxygenation-induced permeability
change occurred in sickle cells only for cations and chloride. Monovalent
cation permeabilities increased five-fold, and chloride influx into DIDS
treated cells was enhanced nearly threefold on sickle cell deoxygenation.
In contrast, no detectable increase in permeability to the other solutes
was found. To gain perspective on these findings, similar measurements were
performed in normal cells treated with diamide, an agent shown by others to
induce a coupled increase in membrane permeability and phospholipid
translocation, reminiscent of deoxygenation-induced changes in sickle
cells. Although the increase in cation permeability was no greater than
that in sickled cells, treatment with 2 mmol/L diamide also produced a
twofold increase in the first order rate constants for sulfate exchange and
mannitol efflux, indicating a relatively nonselective permeability increase
that permitted flux of larger solutes than in the case of deoxygenated
sickle cells. These results suggest that the deoxygenation of sickle cells
induces a permeability increase that is relatively insensitive to charge,
but is restrictive with respect to solute size.
This article has been cited by other articles:
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| Copyright © 1990 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
