Unsaturated aldehydes in plasma, liver and brain of chicken in response to dietary vitamin E and fat type

Abstract Dietary fats modify phospholipid fatty acids (PL-FA) in brain and liver of chicks by post-hatching. Vitamin E deficiency leads to an increase of lipid peroxidation products. Both processes may be relevant to the pathogenesis of chick nutritional encephalomalacia (NE). Laying hens received a diet low in vitamin E (∼10 ppm). Resulting chicks were assigned to four dietary groups each fed with either linoleic (18:2n6, 55g/kg) or linolenic (18:3n3, 54g/kg) acid together with 1 or 50 ppm vitamin E. NE affecting the cerebellum only occurred in the group fed 18:2n6 and 1 ppm vitamin E. After 7, 9, 11 and 13 days the aldehyde concentrations in plasma, liver, cerebrum and cerebellum were determined by GLC. In a concomitant identical experiment the PL-FA contents of liver and brain were measured. Feed fatty acids were incorporated into the liver very efficiently during the second week of life. In the chicken brain the alterations due to dietary lipids were less distinct. An effect of vitamin E supplementation on the over-all PL-FA pattern only occurred in liver. The tissue content of unsaturated aldehydes increased during the second week of life. Aldehyde pattern was widely influenced by the type of dietary fat. Vitamin E deficiency led to elevated aldehyde content only in plasma. Tissue concentration increased when linoleic acid-rich fat was supplied due to a high content of n6-aldehydes, especially OH-nonenal. In liver and cerebrum the n3n6 ratio of aldehydes and PL-FA was comparable. However, in cerebellum the portion of n6 aldehydes was disproportional higher than it was in the PL-FA. This points to a role of cerebellar aldehyde metabolism in the pathogenesis of NE.