Journal of Applied Physiology AJP: Regulatory, Integrative and Comparative Physiology
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J Appl Physiol 67: 1070-1075, 1989;
8750-7587/89 $5.00
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Journal of Applied Physiology, Vol 67, Issue 3 1070-1075, Copyright © 1989 by American Physiological Society

ARTICLES

Blood sulfhydryl level increases during hyperoxia: a marker of oxidant lung injury

C. J. Beehler, M. L. Simchuk, K. M. Toth, S. K. Drake, N. B. Parker, C. W. White, E. M. Berger, R. J. Sanderson and J. E. Repine
Department of Medicine, Webb-Waring Lung Institute, Denver, Colorado.

Blood acid-soluble sulfhydryl, but not glutathione (GSH), levels increased during the development of acute edematous lung injury in rats exposed to normobaric hyperoxia for 48 h or more. A relationship between increases in blood sulfhydryl levels, lung injury, and O2 metabolite generation during exposure to hyperoxia was suggested by two observations. First, increases in blood sulfhydryl levels occurred simultaneously with increases in lung oxidized glutathione (GSSG) levels and lung GSSG-to-GSH ratios (GSSG/GSH). Second, hyperoxia-induced increases in blood sulfhydryl levels, blood hematocrits, pleural effusion volumes, lung GSSG levels, and lung GSSG/GSH were decreased by pretreating rats with dimethylthiourea (DMTU), an O2 metabolite scavenger. Our findings indicate that exposure of rats to hyperoxia increases blood acid-soluble sulfhydryl levels in vivo and that increases in blood sulfhydryl levels may provide an accessible marker of increased oxidant exposure and/or oxidant-mediated lung injury.


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