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To study the ability of different tissues to recover from essential fatty acid deficiency, male rats were maintained for 25 weeks with a diet containing 10% hydrogenated coconut oil and were then transferred to a diet containing 10% corn oil. The total fatty acid compositions of brain, heart and testes lipids were determined at intervals over an 81-day period. Lipids from the deficient animals were low in the linoleic-series acids and high in oleic-series acids. Feeding corn oil to the deficient animals reversed this situation. Linoleic acid was rapidly incorporated into heart lipids, the changes in arachidonic and the higher polyunsaturated acids occurring more slowly. Slightly elevated levels of eicosatrienoic persisted after the concentration of total ω6-acids had returned to normal. Changes in brain fatty acids were slow, reflecting the slow metabolic turnover of lipids in this tissue. Docosahexaenoic acid, which is relatively high in brain lipids, was independent of the initial diet or of the supplemental corn oil diet. Arachidonic acid was more readily incorporated into the testes lipids than any other acid. Docosapentaenoic acid, the major ω6-acid of the testes from control animals, remained at a constant low level for several weeks before increasing to a level greater than that of the controls at 81 days. Both tissue and fatty acid specificities were observed.

To determine the ability of various tissues to incorporate essential fatty acids, rats maintained with a diet deficient in essential fatty acids for 25 weeks were transferred to a diet containing 10% corn oil. The fatty acid compositions of plasma, erythrocyte and liver lipids were determined at intervals over an 81-day period. Lipids from the deficient animals were low in linoleic and arachidonic acids and high in palmitoleic, oleic and eicosatrienoic acids. Supplemental feeding with corn oil resulted in a rapid increase in linoleic and arachidonic acids and decrease in palmitoleic, oleic and eicosatrienoic acids in the plasma and liver, although the latter acid remained above the level in the control animals for a longer period than palmitoleic and oleic acids. In the erythrocyte, linoleic acid was rapidly incorporated and oleic acid lost with equal facility. Incorporation of arachidonic acid, while initially rapid, proceeded throughout the 81 days of the experiment. Loss of eicosatrienoic acid was also a long-term process. The rate of incorporation of essential fatty acids by tissues from deficient rats was a function of each tissue and each fatty acid.

Male rats were fed for 36 weeks diets containing 10% corn oil or 10% hydrogenated coconut oil. The adrenal lipids were extracted, fractionated by column chromatography and the fatty acid composition of the fractions determined by gasliquid chromatography. The major fatty acid in the cholesterol ester fraction from the deficient rats was identified as 7,10,13-docosatrienoic acid (22:3ω9) and this accounted for 25% of the total fatty acids in this fraction. The polyunsaturated acid usually found in tissues from EFA-deficient animals, 5,8,11-eicosatrienoic acid (20:3ω9), constituted 21% of the total adrenal cholesterol ester fatty acids. This pattern in the deficient rats refiected that found in the control animals where 22:4ω6 and 20:4ω6 were the major acids. The structure of the 22:3ω9 acid was confirmed by ozonolysis. Just as the 22:4ω6 acid was characteristic of the adrenal cholesterol esters and was not a major component of the triglycerides or phospholipids of normal animals, no 22:3ω9 acid was found in the triglyceride fraction and very little in the phospholipid fraction from the adrenals of EFA-deficient rats. Arachidonic and 20:3ω9 were the major polyunsaturated acids of the phospholipids from normal and deficient rat adrenals, respectively.

The response of rat erythrocyte fatty acids to 4 fats of widely differing fatty acid compositions was investigated. The red cell fatty acids were susceptible to dietary influence but in a very specific manner. Short-chain dietary fatty acids, provided by butter and hydrogenated coconut oil, were not incorporated into the erythrocyte lipids to any appreciable extent. The “non-mammalian” hydroxy acid, ricinoleic acid, was not incorporated into the cell when castor oil was included in the diet. This was possibly due, in both cases, to the absence from the plasma of significant levels of the acids in question. Diets low in essential fatty acids resulted in low cellular concentrations of linoleic and arachidonic acids, with a concomitant accumulation of oleic and eicosatrienoic acids. The high dietary linoleic acid provided by corn oil resulted in the accumulation of this acid in the cell at the expense of the oleic acid. Fatty aldehydes, derived from the plasmalogen phosphatides, were also responsive to diet, linoleyl aldehyde increasing with increased dietary linoleate.

The lipid composition of rat erythrocyte stroma was studied when corn oil and lard were fed with or without vitamin E supplements. Substitution of lard for corn oil did not influence the relative concentrations of the neutral lipid, or choline- and noncholine-containing phospholipids of the stroma lipids. Gas-liquid chromatography indicated that the noncholine-containing phospholipids were rich in arachidonic acid. Hexadecanal, octadecanal and octadecenal also occurred, presumably in the form of phosphatide plasmalogens. The choline-containing lipids contained more saturated fatty acids, primarily palmitic acid. More linoleic acid occurred in this fraction than in the noncholine phospholipids, whereas the longer-chain-length polyenoic acids were less abundant. Aldehydes were present in lower concentrations, indicating that a smaller fraction of choline phosphatides occurred as plasmalogens. The corn oil diet, rich in linoleic acid, resulted in the occurrence of higher concentrations of this acid and of docosaenoic acids, whereas oleic acid was present in higher concentrations in the phospholipid fatty acids when lard was used as the dietary fat. Arachidonic acid was independent of this dietary variation as were the aldehydes. Vitamin E deficiency appeared to exert no influence on the fatty acid composition of the phospholipids.

Male Wistar rats were fed diets containing 10% corn oil and supplemented with or deficient in pyridoxine. One pyridoxine-supplemented group was pairfed with the deficient group. After 12 weeks, each group was divided into two subgroups which were fed diets containing 10% hydrogenated coconut oil and supplemented or deficient in pyridoxine for 20 weeks. Blood samples were taken from the tail vein at 4-week intervals and erythrocyte fatty acids analyzed. Lack of pyridoxine for the entire experiment resulted in the most rapid loss of erythrocyte arachidonate and incorporation of oleic and eicosatrienoic acids. At the end of the experiment, there was less arachidonic acid and more oleic and eicosatrienoic acids in erythrocyte lipids from this group of rats than from any other group. Animals receiving vitamin B6throughout the experiment exhibited the smallest changes in tissue fatty acid composition. The effects of changing the B6status of the diet in the second phase of the experiment were less well defined. Loss of arachidonic acid from the erythrocyte after imposition of the EFA-deficient diet was more rapid if pyridoxine deficiency accompanied the EFA deficiency rather than preceding it. However, the final concentrations of arachidonic acid did not differ in these two groups.