Fatty acid desaturation in lung: inhibition by unsaturated fatty acids

• Published in: Journal of lipid research 1980-09, Vol.21 (7), p.868-873
• Main Authors: Balint, J A, Kyriakides, E C, Beeler, D A
• Format: Article
• Language: English
• Subjects: 16,16-Dimethylprostaglandin E2 - pharmacology; Animals; Fatty Acid Desaturases - antagonists & inhibitors; Fatty Acids, Essential - deficiency; Fatty Acids, Unsaturated - metabolism; Fatty Acids, Unsaturated - pharmacology; Linoleic Acids - pharmacology; Linolenic Acids - pharmacology; Liver - enzymology; Liver - metabolism; Lung - enzymology; Male; Oleic Acids - pharmacology; Palmitic Acids - pharmacology; Rats
• ISSN: 0022-2275
• DOI: 10.1016/S0022-2275(20)34783-0

The activity of the enzyme system involved in desaturation of palmitic and stearic acid has been examined in lungs of rats fed fat-free diets supplemented either with 4% safflower oil (controls) or 4% tripalmitin (essential fatty acid (EFA) deficient) both in vivo and in vitro in lung slices. Desaturation, as measured by appearance of 14C-labeled monounsaturated fatty acid in pulmonary total lipid and phospholipids, was significantly greater in vivo and in vitro in lung tissue from EFA-deficient rats. In vitro peincubation of lung slices for 1 to 4 hr with 1 mM oleic, linoleic, or linolenic acid reduced the extent of desaturation of [1-14C]-stearic acid significantly in both dietary groups, but the effect was greater in EFA-deficient tissues. The effect of linoleic acid was always greater than that of oleic acid. Preincubation with palmitic acid and 16,16-dimethyl PGE2 was without effect. Thus: 1) EFA deficiency has been shown to enhance desaturation of palmitic and stearic acid in lung; 2) in vitro addition of linoleic or linolenic acid inhibited desaturation significantly; and 3) oleic acid was inhibitory but to a lesser and more variable extent. Palmitic acid was not inhibitory.