Hrboticky N, Sellmayer A, Yeo Y, Pietsch A, Weber P C
Institut für Prophylaxe und Epidemiologie der Kreislaufkrankheiten, Ludwig-Maximilians-Universität, Müncher, Germany.
Biochim Biophys Acta. 1996 Aug 16;1302(3):199-206. doi: 10.1016/0005-2760(96)00062-8.
The cellular metabolism of albumin- and lipoprotein-bound 18:2(n - 6) during monocytic differentiation was examined in the human premonocytic U937 and Mono Mac 6 cells. Differentiation for 72 h of U937 cells with retinoic acid (RA, 1 microM) or 1,25-(OH)2-vitamin D3 (1,25-D3, 10 nM) and of Mono Mac 6 cells with RA (1 microM) or lipopolysaccharide (LPS, 10 ng/ml) increased the desaturation and elongation of [1-14C]18:2(n - 6) to [1-14C]20:4(n - 6). In undifferentiated U937 and Mono Mac 6 cells, incubations with human LDL (100 micrograms/ml, 18 h) resulted in a 2.5-fold increase in 18:2(n - 6) levels in the cellular phospholipids. Differentiation of U937 cells with RA or or of Mono Mac 6 cells with LPS prior to LDL addition. Significantly reduced 18:2(n - 6) and elevated 20:4(n - 6) levels in cellular phospholipids. This increase in 20:4(n - 6) was likely not due to an increased incorporation of preformed 20:4(n - 6) esterified in LDL, as the receptor-specific degradation of [125I]LDL was reduced in both the RA-treated U937 and LPS-treated Mono Mac 6 cells. In U937 cells incubated with [1-14C]18:2(n - 6), the synthesis of TXB2, PGE2 and HHT could be detected after differentiation with RA. suggesting the availability of [1-14C]20:4(n - 6), derived from [1-14C]18:2(n - 6), for cyclooxygenase metabolism. Our results show that the conversion of 18:2(n - 6) to 20:4(n - 6) increases during monocyte differentiation. The 18:2(n - 6) supplied to the cells via the receptor-mediated uptake of LDL was utilized as substrate for the increased 20:4(n - 6) synthesis.
在人早幼单核细胞U937和单核巨噬细胞6细胞中，研究了单核细胞分化过程中与白蛋白和脂蛋白结合的18:2(n - 6)的细胞代谢。用视黄酸（RA，1微摩尔）或1,25-(OH)2-维生素D3（1,25-D3，10纳摩尔）处理U937细胞72小时，以及用RA（1微摩尔）或脂多糖（LPS，10纳克/毫升）处理单核巨噬细胞6细胞72小时，均增加了[1-14C]18:2(n - 6)向[1-14C]20:4(n - 6)的去饱和及延长。在未分化的U937和单核巨噬细胞6细胞中，用人低密度脂蛋白（LDL，100微克/毫升）孵育18小时，导致细胞磷脂中18:2(n - 6)水平增加2.5倍。在添加LDL之前，用RA诱导U937细胞分化或用LPS诱导单核巨噬细胞6细胞分化，可显著降低细胞磷脂中18:2(n - 6)水平，并提高20:4(n - 6)水平。20:4(n - 6)的这种增加可能并非由于LDL中酯化的预先形成的20:4(n - 6)掺入增加，因为在经RA处理的U937细胞和经LPS处理的单核巨噬细胞6细胞中，[125I]LDL的受体特异性降解均减少。在用[1-14C]18:2(n - 6)孵育的U937细胞中，用RA诱导分化后可检测到TXB2、PGE2和HHT的合成，这表明源自[1-14C]18:2(n - 6)的[1-14C]20:4(n - 6)可用于环氧化酶代谢。我们的结果表明，在单核细胞分化过程中，18:2(n - 6)向20:4(n - 6)的转化增加。通过受体介导摄取LDL提供给细胞的18:2(n - 6)被用作增加的20:4(n - 6)合成的底物。
