Dietary fatty acids modify phospholipid fatty acids in brain and liver of growing chickens post-hatching.The effect of vitamin E deficiency on this process is unknown and may be relevant to the pathogenesis of chick nutritional encephalomalacia (NE). Therefore laying hens received a diet low in vitamin E (10 mg α-tocopherol/kg feed). Resulting chicks were assigned to nine dietary groups each fed with either oleic (18:ln-9, 58 g/kg), linoleic (18:2n-6, 57 g/kg) or linolenic (18:3n-3, 56 g/kg) acid together with 5, 25 or 125 mg α-tocopherol/kg feed. NE affecting the cerebellum only occurred in the group given linoleic acid and 5 mg α-tocopherol/kg.In l-d-old chicks and after 1 and 2 weeks the phospholipid fatty acid composition of liver, cerebrum and cerebellum (additionally after 3 weeks) was determined. The feed fatty acids were incorporated into the liver very efficiently during the first week of life. Unsaturation of liver membranes decreased in the orderdietary linolenic >linoleic >oleic acid. In liver, also, the effect of α-tocopherol supplementation on phospholipid fatty acids was most pronounced. Theunsaturation index increased during deficiency, whereas n-9 fatty acids decreased. In the chicken brain the alterations were delayed and less distinct. The cerebellum phospholipids were rich in n-9 fatty acids and as a whole more saturated in comparison with the cerebrum. Cerebellar unsaturation increased when linolenic or linoleic acid was given. However, NE-producing dietary conditions were not accompanied by specific alterations in cerebellar phospholipid fatty acids due to the α-tocopherol content of the diet. Rather the alterations of membrane fatty acids in the liver seem to play a role in the pathogenesis of NE.