Platelets attenuate oxidant-induced permeability in endothelial monolayers: glutathione-dependent mechanisms.
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 increase 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, 1-chloro-2,4-dinitrobenzene, or buthionine sulfoximine 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.
Division of Pulmonary and Critical Care Medicine, Medical University of South Carolina, Charleston 29425, USA.
C
C
Strange
A
A
Gottehrer
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K
Birmingham
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JE
Heffner
D000818:Animals; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D002417:Cattle; D002463:Cell Membrane Permeability / Q000187:drug effects*; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism*; D005949:Glucose Oxidase / Q000633:toxicity; D005978:Glutathione / Q000502:physiology*; D006801:Humans; D016877:Oxidants / Q000633:toxicity*; D010084:Oxidation-Reduction; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D012711:Serum Albumin, Radio-Iodinated
D016877:Oxidants; D010975:Platelet Aggregation Inhibitors; D012711:Serum Albumin, Radio-Iodinated; D005949:Glucose Oxidase; D005978:Glutathione