Journal of Applied Physiology, Vol 62, Issue 2 533-538, Copyright © 1987 by American Physiological Society
Hyperbaric hyperoxia reversibly inhibits erythrocyte phospholipid fatty acid turnover
C. A. Dise, J. M. Clark, C. J. Lambersten and D. B. Goodman
The present study is one component of a comprehensive investigation of
oxygen tolerance of tissues and organs in normal human subjects. The focus
of this study was the acylation of membrane phospholipid in situ by
erythrocytes. Activation of exogenous [9,10-3H]oleic acid to acyl thioester
and transesterification of the acyl thioester into phospholipid by intact
human erythrocytes incubated in vitro decreased 30% after exposure of 10
human subjects to hyperbaric hyperoxia (100% O2, 3 ATA, 3.5 h). Partial
recovery of activity could be detected when additional cells were obtained
from these subjects and assayed in vitro 24 h after cessation of exposure.
No significant change in membrane phospholipid fatty acid composition was
detected under these conditions. The reduced glutathione content of intact
erythrocytes increased by 15% after hyperbaric hyperoxia and remained
elevated 24 h after exposure. In isolated membranes prepared from the same
cells activation of [9,10-3H]oleic acid to acyl thioester and its
transesterification into phospholipid did not change after hyperoxia. Since
the ability of intact cells to replace oxidized fatty acids in membrane
phospholipids via deacylation and reacylation in situ may be necessary for
the maintenance of membrane integrity during exposure to oxidative stress,
the decrease in [9,10-3H]oleic acid incorporation by human erythrocytes
detected in vitro after hyperbaric hyperoxia in vivo may reflect an early
event in the pathogenesis of oxygen-induced cellular injury and may be a
useful index for assessment of the tolerance of tissues to hyperoxia.
