首页> 外文期刊>Fish Physiology and Biochemistry >Essential fatty acid deficiency in freshwater fish: the effects of linoleic, alpha-linolenic, gamma-linolenic and stearidonic acids on the metabolism of [1-14C]18:3n-3 in a carp cell culture model.
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Essential fatty acid deficiency in freshwater fish: the effects of linoleic, alpha-linolenic, gamma-linolenic and stearidonic acids on the metabolism of [1-14C]18:3n-3 in a carp cell culture model.

机译:淡水鱼中必需脂肪酸的缺乏:在鲤鱼细胞培养模型中,亚油酸,α-亚麻酸,γ-亚麻酸和硬脂酸对[1-14C] 18:3n-3代谢的影响。

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摘要

The desaturation of [1-14C]18:3n-3 to 20:5n-3 and 22:6n-3 is enhanced in an essential fatty acid deficient cell line (EPC-EFAD) in comparison with the parent cell line (EPC) from carp. In the present study, the effects of competing, unlabelled C18 polyunsaturated fatty acids (PUFA) (linoleic (18:2n-6), alpha-linolenic (18:3n-3), gamma-linolenic (18:3n-6) and stearidonic (18:4n-3) acids), on the metabolism of [1-14C]18:3n-3 were investigated in EPC-EFAD cells in comparison with EPC cells. The incorporation of [1-14C]18:3n-3 in both cell lines was significantly reduced by competing C18 PUFA, with the rank order being 18:4n-3>18:3n-3=18:2n-6>18:3n-6. In the absence of competing PUFA, radioactivity from [1-14C]18:3n-3 in EPC cells was predominantly recovered in phosphatidylethanolamine followed by phosphatidylcholine. This pattern was unaffected by competing n-6PUFA, but n-3PUFA reversed this pattern as did essential fatty acid deficiency in the presence of all competing PUFA. The altered lipid classdistribution was most pronounced in cells supplemented with 18:4n-3. Competing C18 PUFA significantly decreased the proportions of radioactivity recovered in 22:6n-3, pentaene and tetraene products, with the proportions of radioactivity recovered in 18:3n-3 and 20:3n-3 increased, in both cell lines. However, the inhibitory effect of competing C18 PUFA on the desaturation of [1-14C]18:3n-3 was significantly greater in EPC-EFAD cells. The magnitude of the inhibitory effects of C18 PUFA on [1-14C]18:3n-3desaturation was dependent upon the specific fatty acid with the rank order being 18:4n-3>18:3n-3>18:2n-6, with 18:3n-6 having little inhibitory effect on the metabolism of [1-14C]18:3n-3 in EPC cells. The differential effects of the C18 PUFA on [1-14C]1
机译:与亲本细胞系(EPC)相比,必需脂肪酸缺乏细胞系(EPC-EFAD)增强了[1-14C] 18:3n-3至20:5n-3和22:6n-3的去饱和从鲤鱼。在本研究中,未标记的竞争性C18多不饱和脂肪酸(PUFA)(亚油酸(18:2n-6),α-亚麻酸(18:3n-3),γ-亚麻酸(18:3n-6)和与EPC细胞相比,在EPC-EFAD细胞中研究了[1-14C] 18:3n-3的硬脂酸(18:4n-3)酸的代谢。通过竞争性C18 PUFA,两种细胞系中[1-14C] 18:3n-3的掺入均显着减少,排名顺序为18:4n-3> 18:3n-3 = 18:2n-6> 18: 3n-6。在不存在竞争性PUFA的情况下,EPC细胞中[1-14C] 18:3n-3的放射性主要在磷脂酰乙醇胺中,然后在磷脂酰胆碱中回收。这种模式不受竞争的n-6PUFA的影响,但是n-3PUFA逆转了这种模式,在所有竞争的PUFA存在下,基本脂肪酸缺乏也是如此。脂类分布的改变在补充18:4n-3的细胞中最为明显。在两种细胞系中,竞争性C18 PUFA显着降低了22:6n-3,戊烯和四烯产物中回收的放射性比例,而18:3n-3和20:3n-3中回收的放射性比例增加。但是,在EPC-EFAD细胞中,竞争性C18 PUFA对[1-14C] 18:3n-3脱饱和的抑制作用明显更大。 C18 PUFA对[1-14C] 18:3n-3去饱和的抑制作用的大小取决于特定的脂肪酸,其排列顺序为18:4n-3> 18:3n-3> 18:2n-6, 18:3n-6对EPC细胞中[1-14C] 18:3n-3的代谢几乎没有抑制作用。 C18 PUFA对[1-14C] 1的不同影响

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