Cantrill R C, Huang Y S, Ells G W, Horrobin D F
EFAMOL Research Institute, Kentville, Nova Scotia, Canada.
Lipids. 1993 Mar;28(3):163-6. doi: 10.1007/BF02536634.
The incorporation and metabolism of alpha-linolenic acid (18:3n-3) and its delta 6 desaturase product, stearidonic acid (18:4n-3), were compared by NIH-3T3 cells. In the presence of fetal calf serum, cells accumulated exogenously added 18:3n-3 and 18:4n-3 apparently at the expense of oleic acid (18:1n-9). Both 18:3n-3 and 18:4n-3 were elongated and desaturated to eicosatetraenoic acid (20:4n-3), eicosapentaenoic acid (20:5n-3) and docosapentaenoic acid (22:5n-3), but not to docosahexaenoic acid (22:6n-3), and were incorporated into phospholipids and triacylglycerols. Over a 4-d period, the growth of NIH-3T3 cells was slightly stimulated in the presence of 18:3n-3 (20 micrograms/mL) but was strongly inhibited in the presence of 18:4n-3 at the same concentration. This inhibition may be caused by enhanced lipid peroxidation as a result of the high levels of 18:4n-3 present.
通过NIH-3T3细胞比较了α-亚麻酸(18:3n-3)及其δ6去饱和酶产物十八碳四烯酸(18:4n-3)的掺入和代谢情况。在胎牛血清存在的情况下,细胞明显以油酸(18:1n-9)为代价积累外源性添加的18:3n-3和18:4n-3。18:3n-3和18:4n-3均被延长并去饱和为二十碳四烯酸(20:4n-3)、二十碳五烯酸(20:5n-3)和二十二碳五烯酸(22:5n-3),但未转化为二十二碳六烯酸(22:6n-3),并被掺入磷脂和三酰甘油中。在4天的时间里,在18:3n-3(20微克/毫升)存在的情况下,NIH-3T3细胞的生长受到轻微刺激,但在相同浓度的18:4n-3存在的情况下则受到强烈抑制。这种抑制可能是由于存在高水平的18:4n-3导致脂质过氧化增强所致。