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Exogenous oxidants initiate hydrolysis of endothelial cell inositol
phospholipids
DM Shasby, M Yorek and SS Shasby
Department of Internal Medicine, University of Iowa Hospitals, Iowa City
52242.
Oxidants released from inflammatory cells contribute to the pathogenesis of
acute inflammatory edema in many models. Chemically produced oxidants can
reversibly alter the barrier properties of cultured endothelial and
epithelial monolayers. This report examines the effects of nonlytic doses
of H2O2 on endothelial cell lipids. H2O2 oxidized omega-6 fatty acids in
the endothelial cells and initiated hydrolysis of endothelial cell
phospholipids. When endothelial cells were exposed to peroxidized linoleic
acid, it caused lysis of the cells at doses 1,000-fold lower than effective
doses of H2O2. The phospholipid hydrolysis was directed primarily at the
inositol phospholipids and consisted of both A and C type phospholipase
activity. The phospholipase A hydrolysis resulted in increases in
endothelial cell free fatty acids and lysophosphatidylinositol. The
phospholipase C hydrolysis resulted in increases in diglycerides,
phosphatidic acid, and inositol polyphosphate levels. The phospholipase C
hydrolysis of phosphatidylinositol is known to activate protein kinase C in
most cells. Stimulation of protein kinase C with phorbol- 12,13-dibutyrate
increased albumin flux across endothelial monolayers and altered
endothelial cell shape, similar to effects of oxidants. These data are
consistent with the hypothesis that oxidant-initiated hydrolysis of
endothelial cell inositol phospholipids contributes to oxidant-mediated
reversible changes in endothelial monolayer barrier function.
Volume 72,
Issue 2,
pp. 491-499,
08/01/1988
Copyright © 1988 by The American Society of Hematology
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