Yousef I M, O'Doherty P J, Whitter E F, Kuksis A
Lab Invest. 1976 Mar;34(3):256-62.
Sucrose gradient sedimentation and electron micrographic studies were made on the ribosomes of the cells of intestinal mucosa isolated from control, bile fistula, and puromycin-treated rats. In comparison to controls, there was a 40 to 60 per cent decrease in polysome content of the cells following administration of puromycin or deprivation of luminal choline by creation of a bile fistula. Feeding of lysolecithin of choline to the bile fistula rats or addition to the isolated cells in vitro resulted in a complete restoration of the polysome profile along with lipprotein synthesis and chylomicron release. Addition of lysolecithin to isolated cells treated with puromycin in vitro also brought about a reaggregation of the ribosomes and a reactivation of phospholipid biosynthesis. Choline had no detectable effect on phospholipid synthesis or ribsosme aggregation when fed to ppuromycin-treated rats or when added to puromycin-treated cells in vitro. The results suggest that chylomicron formation and the release by the muscosal cells depend upon intact rough endoplasmic reticulum and an active protein adn phospholipid biosynthesis. The role of lysolecithin in this process is ratonalized on the basis of its ability to supply a precursor of lecithin as well as a surfactant which affects the aggregation, or membrane rebinding of ribosomes, or both.
对从对照大鼠、胆瘘大鼠和经嘌呤霉素处理的大鼠分离出的肠粘膜细胞核糖体进行了蔗糖梯度沉降和电子显微镜研究。与对照相比，给予嘌呤霉素或通过建立胆瘘剥夺腔内胆碱后，细胞中的多核糖体含量降低了40%至60%。给胆瘘大鼠喂食溶血卵磷脂或胆碱，或在体外向分离的细胞中添加溶血卵磷脂或胆碱，可使多核糖体图谱完全恢复，同时脂蛋白合成和乳糜微粒释放也恢复。在体外向经嘌呤霉素处理的分离细胞中添加溶血卵磷脂，也会导致核糖体重新聚集和磷脂生物合成重新激活。当给经嘌呤霉素处理的大鼠喂食胆碱或在体外将胆碱添加到经嘌呤霉素处理的细胞中时，胆碱对磷脂合成或核糖体聚集没有可检测到的影响。结果表明，乳糜微粒的形成和粘膜细胞的释放取决于完整的粗面内质网以及活跃的蛋白质和磷脂生物合成。溶血卵磷脂在这一过程中的作用基于其提供卵磷脂前体以及影响核糖体聚集或膜重新结合或两者的表面活性剂的能力而得到合理化解释。
