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The influences of early changes in essential fatty acid deficiency on the structure and metabolism of lung phosphatidylcholine were studied. In addition to general characteristics observed due to essential fatty acid deficiency such as significant decreases in linoleate and arachidonate, and concomitant increases in oleate and eicosatrienoate, a pronounced decrease in palmitate was noted in lung phosphatidylcholine, particularly in the 2-position. The decrease of palmitate in lung phosphatidylcholine was due to a similar decrease in disaturated classes, particularly in the dipalmitoyl species. These structural changes in phosphatidylcholine were found to be more significant in alveolar wash than in lung parenchyma and lamellar body fractions. The specific activities of phosphatidylcholine and its disaturated classes in lung parenchyma and alveolar wash were significantly lower in the deficient state than in the controls at 2, 6, and 12 hr after the injection of [9,10(-3)H]palmitate. However, relatively more of the phosphatidylcholine in the deficient state appeared in the alveolar space, disappearing more rapidly from the alveolar space than did the phosphatidylcholine in the controls. These results suggest that dietary linoleate may be a factor in regulating the amount of disaturated phosphatidylcholine in the lung, a principal component of lung surfactant, and also a factor in controlling the metabolism of alveolar phosphatidylcholine.

Structural and metabolic alterations of lung phosphatidylcholines by essential fatty acid deficiency.