The encephalomalacia producing effect of arachidonic and linoleic acids.

Abstract

Vitamin E-free diets containing 1.5% of the ethyl estera of linoleic and arachidonic acids, respectively, and a vitamin E-free diet containing 30% lard were fed to groups of 10 chicks from the age of 5 days through a period of maximally 35 days. All chicks in the arachidonate group developed encephalomalacia within 13 days. In the linoleate group, encephalomalacia began after 13 days. A total of 7 of the chicks in this group had encephalomalacia at the end of the feeding period. In the group receiving 30% lard, encephalomalacia developed somewhat faster than in the linoleate group but slower than in the arachidonate group. Earlier experiments in which 1.5% of ethyl linoleate and 1.5% of ethyl linolenate were compared showed that ethyl linolenate did not give rise to encephalomalacia within the feeding period. The integrity of that part of the linoleic acid molecule comprising the 10 last carbon atoms (counted from the carboxyl group) seems to be of importance for the development of encephalomalacia. A corresponding structure is present in arachidonic but not in linolenic acid. The additional unsaturation of arachidonic acid may contribute to the superiority of this fatty acid as encephalomalacia producing agent. Further, it is possible that the encephalomalacia producing effect of dietary linoleic acid is mediated by arachidonic acid formed in the tissues from the ingested linoleic acid. The possibility of explaining the development of encephalomalacia on the basis ofin vivo autoxidation of fatty acids is discussed.