Berkovic D, Grunwald U, Menzel W, Unger C, Hiddemann W, Fleer E A
University Clinic of Göttingen, Department of Internal Medicine, Germany.
Eur J Cancer. 1995 Nov;31A(12):2080-5. doi: 10.1016/0959-8049(95)00350-9.
Hexadecylphosphocholine (HePC) is an analogue of the antiproliferative alkyllysophospholipids (ALP). As these lipid-like compounds interfere with membrane lipid metabolism at several sites, we studied the effects of HePC on uptake and metabolism of inositol and choline, two important phospholipid precursor molecules in two sensitive cell lines, Raji and KB, and in a resistant variant of KB cells, KBr. HePC substantially inhibited the membrane uptake of inositol and of choline in KB and Raji. Inositol uptake of KBr cells was constitutively low and was not further decreased by HePC. In all three cell lines, uptake inhibition of choline was less pronounced. Uptake inhibition showed characteristics of a non-specific effect, probably due to the physicochemical properties of HePC as a "lyso" structure. Decreased uptake of inositol did not affect phosphoinositide synthesis. Cellular phosphatidylcholine (PC) metabolism seemed to be affected through inhibition of choline incorporation and enhancement of PC degradation in the two sensitive cells. In KBr cells, these effects were not observed.
十六烷基磷胆碱（HePC）是抗增殖烷基溶血磷脂（ALP）的类似物。由于这些类脂化合物在多个位点干扰膜脂代谢，我们研究了HePC对肌醇和胆碱摄取及代谢的影响，肌醇和胆碱是两种重要的磷脂前体分子，我们选用了两种敏感细胞系Raji和KB以及KB细胞的耐药变体KBr进行研究。HePC显著抑制了KB和Raji细胞中肌醇和胆碱的膜摄取。KBr细胞的肌醇摄取本就较低，HePC不会使其进一步降低。在所有三种细胞系中，胆碱摄取的抑制作用不太明显。摄取抑制表现出非特异性效应的特征，这可能是由于HePC作为“溶血”结构的物理化学性质所致。肌醇摄取的减少并未影响磷酸肌醇的合成。在两个敏感细胞中，细胞磷脂酰胆碱（PC）代谢似乎受到胆碱掺入抑制和PC降解增强的影响。在KBr细胞中，未观察到这些效应。
