LIPID OXIDATION-PRODUCTS AND CHICK NUTRITIONAL ENCEPHALOPATHY
LIPID OXIDATION-PRODUCTS AND CHICK NUTRITIONAL ENCEPHALOPATHY
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DOI：
10.1007/bf02533514
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发表时间：
1979-01-01
期刊：
影响因子：
1.9
通讯作者：
FRANKEL, EN
中科院分区：
文献类型：
--
作者：
BUDOWSKI, P;BARTOV, I;FRANKEL, EN
将红花油及其蒸馏甲酯热氧化后，饲喂维生素E缺乏的雏鸡。在饲粮水平为10%时，氧化脂类比未氧化甲酯类引起的营养性脑病（NE）更为严重；这表明除饲料中的亚油酸和维生素E外，还有其他因素影响NE的发育。氧化甲酯的极性脂质提取物加速了NE的诱导，酮十八烯酸和酮十八烯酸的合成甲酯也加速了NE的诱导。双双酚胺对NE有保护作用。氧化油提供的共轭酮多烯脂肪酸或维生素E缺乏时内源性形成的共轭酮多烯脂肪酸可能在引起NE中起作用。
Safflower oil and its distilled methyl esters were thermally oxidized and fed to young chicks in a vitamin E deficient diet. At a dietary level of 10%, the oxidized lipids caused more severe nutritional encephalopathy (NE) than the unoxidized methyl esters; this indicates that factors other than dietary linoleic acid and vitamin E affect the development of NE. A polar lipid extract from oxidized methyl esters accelerated the induction of NE as did the synthetic methyl esters of keto-octadecenoic and keto-octadecadienoic acids. Dicumarol exerted a protective action against NE. Conjugated keto-polyenoic fatty acids provided by oxidized oils or formed endogenously in vitamin E deficiency may play a role in causing NE.