No abstract

1-Palmitoyl phosphatidylcholines (1-palmitoyl PCs), in which the 2-position was occupied respectively by C10:0, C12:0, C14:0, C14:1, n-7, C16:0, C16:1, n-7, C18:0, C18:1(t), n-9, C18:1, n-9, C18:2, n-6, C18:3, N-3, C18:3, n-6, C18:3(5t,9,12), C22:0, C22:1, n-9, C22:2, n-6, C22:3, n-3, C22:4, n-6, C22:5, n-6 or C22:6, n-3 fatty acids, were studied as monolayer films at the air/water interface. Results for molecular area indicated that the areas of the PC (phosphatidylcholine) did not continuously decrease as the length of one chain increased. For series of saturated, monoenoic and dienoic 1-palmitoyl PCs the smallest molecular area was occupied by the PC containing a 20-carbon acid at the 2-position. In the 18-carbon series, introduction of the first and third cis double bonds caused a large increase in molecular area, but in the 22-carbon series the first and second cis double bonds produced large increases in molecular area. Molecules containing three or more cis double bonds varied little in molecular area, regardless of chain length (18-22 carbon atoms). The influence of a trans double bond was intermediate between that of a saturated and a cis double bond. The 18- and 22-carbon series of PCs were studied in mixed monolayers with cholesterol and desmosterol. Condensation of molecular areas occurred in all sterol PC mixed films, and similar results were obtained with cholesterol and desmosterol. Condensation of PC containing a cis or trans double bond within 10 carbon atoms of the carboxy group initially increased with increasing surface pressure. Condensation of other PCs decreased as surface pressure increased. All cis- or trans-unsaturated PCs condensed maximally in mixtures of approximately equimolar ratios with sterols, but saturated PCs condensed to the greatest extent in mixtures that contained about 30 mol% sterol.

Rats were fed for two generations a purified, linolenic acid-deficient diet in which the only source of lipid was purified methyl linoleate. This diet contained about 38 mg linolenic acid/kg diet. Control rats were given the same diet supplemented with methyl linolenate (2,500 mg/kg diet). Male and female rats ranged in age from weaning pups to adults. Lipids were extracted from liver, brain, kidney, spleen, heart, muscle, gastrointestinal tract, lung, ovary, testis, adrenal, plasma, erythrocytes, retina, and adipose tissue. Fatty acids of major phospholipid classes (choline phosphoglycerides, ethanolamine phosphoglycerides, and mixed serine phosphoglycerides plus inositol phosphoglycerides) or of total lipid extracts were measured by gas liquid chromatography. Growth rates and organ weights were similar in control and linolenic acid-deficient rats. The major effect of the deficiency was to lower the proportions of n-3 fatty acids, especially 22:6 n-3, in all the organs analyzed. Docosahexaenoic acid (22:6 n-3) was mainly replaced by 22:5 n-6 in deficient rats. The greatest changes in composition were found in brain, heart, muscle, retina, and liver.

No abstract

Linolenic acid deficiency has not been demonstrated clearly in warm blooded animals, yet circumstantial evidence suggests that n-3 fatty acids may have functions in these animals. The fact that several species of fish definitely require dietary n-3 fatty acids indicates that n-3 fatty acids have important and specific functions in these animals and suggests that such functions may also be present in warm blooded animals. It is also true that n-3 fatty acid distribution in tissues of birds and mammals appears to be under strict metabolic control, and that this complex metabolic control mechanism apparently has survived evolutionary pressure for a very long time. So far, attempts to produce linolenic acid deficiency in mammals have not revealed an absolute requirement for n-3 fatty acids. If functions for n-3 fatty acids do exist in warm blooded animals, it seems probable that they may be located in the cerebral cortex or in the retina, because these tissues normally contain high concentrations of n-3 fatty acids.