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Transient changes in erythrocyte membrane permeability are induced by
sublytic amounts of the complement membrane attack complex (C5b-9)
JA Halperin, A Taratuska, M Rynkiewicz and A Nicholson-Weller
Department of Medicine, Brigham and Women's Hospital, Boston, MA.
We have previously shown that sublytic heterologous complement induces
large but transient increases in erythrocyte membrane permeability. We now
report that when erythrocytes are bystanders in zymosan-activated
autologous serum, they increase their Na+ permeability 10-fold, indicating
that autologous complement can also induce transient membrane lesions. When
we isolated the effect of the C5b-9 membrane attack complex of complement
by using human C5b-9 assembled from purified components, we found there was
minimal lysis but efficient Na+ uptake. Suspension of the sublytically
damaged erythrocytes in K+ medium caused the cells to lyse, which is
consistent with the cells recruiting a compensatory K+ efflux similar to
that observed when human erythrocytes were exposed to heterologous
complement. Sublytic C5b-9 exposure also became lytic when extracellular
Ca2+ was limited and when the cells were exposed to charybdotoxin, an
inhibitor of the Ca(2+)- activated K+ channel. This indicates that Ca2+ is
required for the functional termination of the C5b-9 lesion. We also show
that the membrane hyperpolarization resulting from activation of the
Ca(2+)- dependent K+ efflux does not influence the termination of the C5b-9
lesion. Thus, the influx of Ca2+ through the complement lesion initiates at
least two apparently independent adaptive responses: (1) a process that
terminates the leak; and (2) a K+ efflux that has a volume regulatory
function. Our data support the potential of the sublytic C5b- 9 lesion to
act as a physiologic mediator for autologous erythrocytes.
Volume 81,
Issue 1,
pp. 200-205,
01/01/1993
Copyright © 1993 by The American Society of Hematology
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