Iron deficiency and neutrophil function: different rates of correction of
the depressions in oxidative burst and myeloperoxidase activity after iron
treatment
H Murakawa, CE Bland, WT Willis and PR Dallman
The polymorphonuclear granulocyte (PMN) kills ingested bacteria by
mechanisms that include myeloperoxidase (MPO) and a sudden increase in
oxygen consumption (the oxidative burst), both of which are iron dependent.
The magnitude of the oxidative burst and activity of MPO were determined in
PMNs during the progression of iron deficiency (ID) and following its
treatment in rats. As ID developed, the oxidative burst after zymosan
activation was less depressed than the activity of MPO. There was no change
in the oxidative burst after activation with phorbol myristate acetate
(PMA) or in the generation of superoxide (O2- ) by NADPH oxidase-containing
particles from PMNs. Following iron treatment, impairment of the oxidative
burst after zymosan activation was corrected after 1 day. In contrast, the
deficit in MPO activity was not corrected until 7 days after initiation of
iron treatment. The pattern of recovery in MPO activity after iron
treatment corresponded to the prolonged period of maturation of the PMN
primary granule since the formation of primary granules, which contain MPO,
takes place only in the early, mitotic stages of maturation. The tendency
of the PMN to maintain the oxidative burst allows the cell to preserve its
capacity for bacterial killing during the progression of iron deficiency.
Volume 69,
Issue 5,
pp. 1464-1468,
05/01/1987
Copyright © 1987 by The American Society of Hematology
