Shichiri G, Kinoshita M, Saeki Y
Central Research Laboratory, Shiga University of Medical Science, Japan.
Arch Biochem Biophys. 1993 Jun;303(2):231-7. doi: 10.1006/abbi.1993.1277.
The mechanism of the antiatherogenic activity of n-3 polyunsaturated fatty acids is not well understood. In these studies, we studied the metabolism of unsaturated fatty acids in murine macrophage-like J774A.1 cells. The major metabolic pathway of 18- and 20-carbon chain unsaturated fatty acids in these cells is the sequence of 2-carbon chain elongation, successive two steps of delta 8- and delta 5-desaturation, and additional elongation. Polyunsaturated fatty acids, arachidonic acid [20:4 (n-6)] and eicosapentaenoic acid [20:5 (n-3)], are elongated into 22:4 (n-6) and 22:5 (n-3) fatty acids, respectively. Accumulation of 22:4 (n-6) and 22:5 (n-3) fatty acids shows that J774A.1 cells have an active chain elongation activity, but lack delta 4-desaturase activity. Furthermore, J774A.1 cells demonstrated almost negligible delta 6-desaturase activity. Enrichment of the membrane lipids of J774A.1 cells with polyunsaturated fatty acids, arachidonic acid [(20:4 (n-6)] and eicosapentaenoic acid [(20:5 (n-3)], increased membrane fluidity and decreased the uptake of acetylated low density lipoprotein.
n-3多不饱和脂肪酸的抗动脉粥样硬化活性机制尚未完全明确。在这些研究中，我们研究了鼠巨噬细胞样J774A.1细胞中不饱和脂肪酸的代谢情况。这些细胞中18碳和20碳链不饱和脂肪酸的主要代谢途径是2碳链延长、连续两步的δ8-和δ5-去饱和以及额外的延长。多不饱和脂肪酸，花生四烯酸[20:4(n-6)]和二十碳五烯酸[20:5(n-3)]，分别延长为22:4(n-6)和22:5(n-3)脂肪酸。22:4(n-6)和22:5(n-3)脂肪酸的积累表明J774A.1细胞具有活跃的链延长活性，但缺乏δ4-去饱和酶活性。此外，J774A.1细胞的δ6-去饱和酶活性几乎可以忽略不计。用多不饱和脂肪酸花生四烯酸[(20:4(n-6)]和二十碳五烯酸[(20:5(n-3)]富集J774A.1细胞的膜脂，可增加膜流动性并减少乙酰化低密度脂蛋白的摄取。
