A 1 carbon degradation of the long chain fatty acids of brain sphingolipids.
A 1 carbon degradation of the long chain fatty acids of brain sphingolipids.
复制标题
脑鞘脂长链脂肪酸的 1 碳降解。
DOI：
10.1016/s0021-9258(18)81113-9
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发表时间：
1963
期刊：
影响因子：
--
通讯作者：
G. Levis
中科院分区：
文献类型：
--
作者：
J. Mead;G. Levis
Since the classical work of Knoop (2) and the elucidation of the details of his P-oxidation mechanism in the laboratories of Green (3), Lynen (4), and others, the primary mode of degradation of fatty acids in the animal body has been well understood. An additional oxidation mechanism, the w-oxidation of Verkade and Van der Lee (5), has been shown to apply under certain special circumstances. The mechanism of biosynthesis of the long chain fatty acids is also approaching clarity with the culmination of work from the laboratories of Wakil (6) and Lynen (7).None of these mechanisms, however, provides a ready explanation for the formation of the C20 to Cz6 ar-hydroxy and odd chain fatty acids of the brain sphingolipids. To explain the presence of these unusual acids, either synthetic or degradative mechanisms may be invoked. The synthesis of odd chain acids from propionate, as proposed by Hajra and Radin (8), has been shown to occur readily with systems in vitro, but it is apparently of minor importance in the whole animal, in which propionate competes unfavorably with acetate (9). A 1 carbon degradative process, on the other hand, although unknown for higher animals, is attractive because it could include the cu-hydroxy acids as intermediates in the formation of the odd chain acids. The a-hydroxy acids were recently shown by Fulco and Mead (10) to be formed by direct hydroxylation of the preformed, unsubstituted long chain acids.
