Platelets attenuate oxidant-induced permeability in endothelial
cell monolayers - glutathione-dependent mechanisms.
Strange, Charlie, Andrew Gottehrer, Karen Birmingham, John E. Heffner.
Division of Pulmonary and Critical Care Medicine, Medical
University of South Carolina, Charleston, SC and Department of
Medicine, St. Joseph's Hospital, Phoenix, AZ
APStracts 3:0261A, 1996.
We studied the effects of adding washed human platelets or platelets
with nonintact glutathione redox cycles to endothelial cell
monolayers treated with glucose oxidase to initiate oxidant stress
and increased permeability. Changes in 125I-labeled albumin
transmonolayer movement were used as the index of monolayer
permeability. Washed human platelets attenuated oxidant-induced
increases in albumin flux. Platelets treated with 1,3-bis(2
-chloroethyl)-1-nitrosurea (BCNU), 1-chloro-2,4-dinitro-benzene
(CDNB), or buthionine sulfoximine (BSO) to inhibit selective
enzymatic steps in the glutathione redox cycle decreased permeability
to a lesser degree. We conclude that 1) washed human platelets
attenuate monolayer permeability defects in aortic endothelial
monolayers exposed to glucose oxidase; and 2) the protective effects
of platelets are partially dependent on an intact platelet
glutathione redox cycle.
Received 5 August 1994; accepted in final form 1 May 1996.
APS Manuscript Number A810-4.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 June 96