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  • Title: Normobaric hyperoxia in vivo inhibits fatty acid incorporation into sheep erythrocyte phospholipid in vitro.
    Author: Dise CA, Hansen-Flaschen J, Lanken PN, Goodman DB.
    Journal: J Lab Clin Med; 1985 Jan; 105(1):89-93. PubMed ID: 3968468.
    Abstract:
    Oxygen toxicity is a major complication of normobaric hyperoxia in therapeutic settings. Because alterations in membrane function occurring as a consequence of peroxidation of membrane phospholipid fatty acids may be an early event in the pathogenesis of oxygen-induced injury, we studied the effects of hyperoxia on the ability of the membrane to repair itself by incorporating fatty acid via the pathway for deacylation and reacylation in situ. Although the lung is the major site of clinically significant injury, the erythrocyte is also directly exposed to elevated PO2 in vivo. In this study, incorporation of [9,10(-3)H]-oleic acid into phospholipid has been measured in sheep erythrocytes in vitro after exposure of four animals to normobaric hyperoxia in vivo. [9,10(-3)H]-Oleic acid incorporation into erythrocyte phospholipid decreased within 24 hours and reached 50% of pre-exposure levels after 70 hours of exposure to 100% O2. No significant change in the fatty acid composition of membrane phospholipid was detected under these conditions. In contrast to the results with intact cells, incorporation of [9,10(-3)H]-oleic acid into phospholipid by isolated erythrocyte membranes prepared from the cells of two animals increased after 70 hours of exposure to 100% O2, indicating that the inhibition of fatty acid incorporation in intact erythrocytes does not result from irreversible inactivation of the enzymes involved in acylation of endogenous lysophospholipid. Because the ability of cells to replace membrane phospholipid fatty acids via deacylation and reacylation in situ could be important in the maintenance of membrane integrity during oxidative stress, the decrease in fatty acid incorporation by erythrocytes in vitro may reflect an early event in the pathogenesis of oxygen-induced cellular injury.
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