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脂质氧化产物与雏鸡营养性脑病

Lipid oxidation products and chick nutritional encephalopathy.

作者信息

Budowski P, Bartov I, Dror Y, Frankel E N

出版信息

Lipids. 1979 Sep;14(9):768-72. doi: 10.1007/BF02533514.

Abstract

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, indicating 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. The possibility is discussed that conjugated keto-polyenoic fatty acids, provided by oxidized oils or formed endogenously in vitamin E deficiency, may play a role in causing NE.

摘要

红花油及其蒸馏甲酯进行热氧化处理后,添加到缺乏维生素E的雏鸡日粮中。日粮中氧化脂质含量为10%时,与未氧化的甲酯相比,其导致的营养性脑病(NE)更为严重,这表明除日粮亚油酸和维生素E外,其他因素也会影响NE的发展。氧化甲酯的极性脂质提取物以及酮基十八碳烯酸和酮基十八碳二烯酸的合成甲酯均能加速NE的诱发。双香豆素对NE具有保护作用。文中讨论了氧化油提供的或在维生素E缺乏时内源性形成的共轭酮多烯脂肪酸可能在导致NE方面发挥作用的可能性。

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