Brain, liver and plasma unsaturated aldehydes in nutritional encephalomalacia of chicks.
Vitamin E deficiency and linoleic acid-feeding lead to nutritional encephalomalacia (NE) in chicks, affecting the cerebellum exclusively. The relevance of lipid peroxidation (LPO) products to the pathogenesis of the disease was studied. Laying hens received a diet low in vitamin E. Resulting chicks were assigned to four groups fed either with linoleic (C18: 2n-6) or linolenic (C18: 3n-3) acid together with 1 or 50 p.p.m. vitamin E. Nine days post-hatching NE occurred in the vitamin E-deficient group fed linoleic acid. With each chick showing NE, a healthy one from all four groups was killed. Unsaturated aldehydes were determined in plasma, liver, cerebrum and cerebellum. Results underlined that the type of dietary fat is decisive for the aldehyde pattern. In the liver of linoleic acid-fed animals total aldehydes were increased. Diseased animals had increased aldehydes stemming from n-3 fatty acids. In plasma, vitamin E deficiency led to higher malondialdehyde and OH-nonenal concentrations. In brain, neither vitamin E deficiency nor NE were accompanied by increased aldehyde concentrations. In consequence a direct role of unsaturated aldehydes for the development of NE in the cerebellum is not probable.[1]References
- Brain, liver and plasma unsaturated aldehydes in nutritional encephalomalacia of chicks. Fuhrmann, H., Sallmann, H.P. Journal of veterinary medicine. A, Physiology, pathology, clinical medicine. (2000) [Pubmed]
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