Neutrophils mediate lipid peroxidation in human red cells
S Claster, DT Chiu, A Quintanilha and B Lubin
Activated neutrophils (ANs) are known to release reactive oxygen species
that may cause oxidative damage to surrounding tissues. We determined if
ANs could induce lipid peroxidation (LP) in human red cells and
investigated the mechanism involved in this interaction. We studied
neonatal glucose-6-phosphate dehydrogenase (G6PD) deficient, and sickle red
cells, since each of these are known to be susceptible to oxidant injury.
Neutrophils were isolated from whole blood and activated by incubation with
opsonized zymosan. Mixtures of such neutrophils and red cells at a ratio of
1:100 were incubated for two hours at 37 degrees C, after which the
malonyldialdehyde content in red cells was measured as an index of LP. All
red cells underwent LP after AN treatment, and the degree of LP was
proportional to the amount of AN in the mixture. Superoxide dismutase and
catalase partially inhibited LP. When compared to normal red cells, only
sickle cells demonstrated a significant increase in AN-mediated LP.
Conversion of hemoglobin to carboxy-hemoglobin increased AN-mediated LP,
whereas conversion to met- hemoglobin decreased AN-mediated LP. The
protective effect of met- hemoglobin on LP was less in sickle cells than in
normal cells. We conclude that AN can induce LP in red cells in vitro and
that sickle cells are more susceptible to this process than normal cells.
Hemoglobin can serve as an electron trap and protect the cell against
peroxidative damage, but this mechanism is impaired in sickle cells. We
speculate that the pathogenesis of hemolysis associated with infectious
disease may include AN-induced red cell LP.
Volume 64,
Issue 5,
pp. 1079-1084,
11/01/1984
Copyright © 1984 by The American Society of Hematology
