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Oxidation-induced changes in microrheologic properties of the red blood
cell membrane
RP Hebbel, A Leung and N Mohandas
Department of Medicine, University of Minnesota, Minneapolis 55455.
It has been hypothesized that some of the irreversible microrheologic
abnormalities of sickle red blood cell (RBC) membranes could result from
autoxidative perturbation. To model this possibility, we used
micromechanical manipulation to examine the static extensional rigidity and
inelastic or plastic behavior of normal RBCs exposed to phenazine
methosulfate (PMS), an agent that generates superoxide from within the
cell. In response to this stress, RBC membranes became stiff as evidenced
by increasing extensional rigidity. At 50 mumol/L PMS they were as stiff as
the membranes of most dense, dehydrated sickle RBCs; and at 25 mumols/L PMS
the membranes were similar to somewhat less dense sickle RBCs. When
examined for inelastic behavior, RBCs exposed to PMS even at 10 mumols/L
showed hysteresis in loading and unloading phases of the curve relating
aspiration length to suction pressure, and they developed membrane bumps
that persisted after RBC release from the pipette. Examination of single
cells in both isotonic and hypotonic buffers showed that the effect of PMS
on RBC microheology is not mediated by cellular dehydration. Independent
confirmation of the membrane stiffening effect of PMS was obtained by
ektacytometric analysis of resealed RBC ghosts, with sickle-like increases
in membrane rigidity observed between 50 and 100 mumol/L PMS. The rigidity
of these ghosts was partially ameliorated by exposure to a thiol reductant.
In terms of biochemical abnormalities, treated RBCs became significantly
different from control RBCs at 25 mumol/L PMS, at which point they just
began to enter the sickle range for amounts of membrane thiol oxidation and
membrane-associated heme. The sickle average was achieved at 50 mumol/L PMS
(for thiol oxidation) to 100 mumol/L PMS (for membrane heme). Thus,
micromolar concentrations of PMS induce abnormalities of membrane
microrheology that closely mimic those of unmanipulated sickle RBCs while
reproducing similar degrees of oxidative biochemical change. We conclude
that membrane protein oxidation could explain existence of an irreversible
component to the abnormal rheology of the sickle membrane.
Volume 76,
Issue 5,
pp. 1015-1020,
09/01/1990
Copyright © 1990 by The American Society of Hematology
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