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Oxidants, ATP depletion, and endothelial permeability to macromolecules
J Wilson, M Winter and DM Shasby
Department of Internal Medicine, University of Iowa College of Medicine,
Iowa City 52242.
Oxidants can reversibly increase the permeability of endothelium to ions
and macromolecules. Oxidants also deplete ATP in cultured endothelial
cells. We asked if oxidant-mediated ATP depletion, alone, accounted for the
effects of oxidants on endothelial permeability to macromolecules. When
porcine pulmonary artery endothelial cells were exposed to 2.5 mmol/LH2O2,
ATP was depleted to 31.7% +/- 1.8% of control within 15 minutes and was
reduced to 23.1% +/- 2.0% of control after 30 minutes. To determine if this
magnitude of ATP depletion could account for the oxidant-induced increase
in endothelial permeability to macromolecules, we measured ATP in
endothelial cells exposed to metabolic inhibitors of ATP production. We
then measured the effects of these metabolic inhibitors on endothelial
monolayer permeability to macromolecules. ATP levels were reduced to 44%
+/- 4% of control by 12 mmol/L deoxyglucose (DOG) in the absence of glucose
and to 2% +/- 1.3% of control by DOG with 25 nmol/L antimycin A in the
absence of glucose. Reduction of endothelial cell ATP to these levels with
the metabolic inhibitors did not alter the flux of albumin or dextran
across the endothelial monolayers. Thus ATP depletion, by itself, does not
explain oxidant-induced changes in endothelial permeability to
macromolecules.
Volume 76,
Issue 12,
pp. 2578-2582,
12/15/1990
Copyright © 1990 by The American Society of Hematology
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