Hale J E, Schroeder F
Eur J Biochem. 1982 Mar 1;122(3):649-61. doi: 10.1111/j.1432-1033.1982.tb06488.x.
A new method for measurement of transbilayer distribution of sterol in plasma membranes is reported. The procedure utilized a fluorescent sterol, dehydroergosterol, and a chemical quenching agent, trinitrobenzenesulfonic acid. Dehydroergosterol was useful as a probe molecule for sterols for the following reasons, (a) Dehydroergosterol contained no bulky side chains as reporter groups. (b) Dehydroergosterol structurally resembled cholesterol and desmosterol, the primary sterol synthesized by LM fibroblasts. (c) Dehydroergosterol interacted with digitonin, filipin, and served as a substrate for cholesterol oxidase. (d) The phase transition of dipalmitoylglycerophosphocholine was completely abolished by dehydroergosterol. (e) The native sterol of LM fibroblasts, desmosterol, was completely replaced by dehydroergosterol without effect on LM cell growth, cell doubling time, plasma membrane (Na+, K+)-ATPase and 5'-nucleotidase activity, microsomal NADPH-dependent cytochrome c reductase activity, and mitochondrial succinate-dependent cytochrome c reductase activity. (f) Neither the phospholipid composition nor the sterol/phospholipid ratio of LM fibroblasts were altered by supplementation with dehydroergosterol. The trinitrophenyl group of trinitrophenylglycine or of surface membranes of LM fibroblasts or red blood cells treated with trinitrobenzenesulfonic acid was an excellent quencher of dehydroergosterol fluorescence. Fluorescence in mouse very-low-density lipoproteins, LM fibroblasts plasma membranes, red blood cell surface membranes, and in rat red blood cell membranes was quenched 95 +/- 3%, 20 +/- 2%, 75 +/- 4%, and 69 +/- 4% respectively when the quenching agent was present on only the extracellular site of the membrane. Trinitrophenyl residues effectively quenched the dehydroergosterol fluorescence in the plasma membrane of LM cells by 20% when dehydroergosterol was present from 1-85 mol/100 ml of the membrane sterol. When both sides of the plasma membrane were trinitrophenylated, greater than 95% of the dehydroergosterol fluorescence was quenched. In addition, when LM cells were cultured with dehydroergosterol, exposed latex beads, and the endocytosed particles isolated as phagosomes and treated with trinitrobenzenesulfonic acid under non-penetrating conditions, the fluorescence of the dehydroergosterol was quenched nearly 64%. From these and other results we deduced that the inner monlayer of the LM fibroblasts plasma membrane was enriched with dehydroergosterol. In contrast, the distribution of the sterol in red blood cell membranes indicated an enrichment in the outer monolayer.
本文报道了一种测量质膜中甾醇跨膜分布的新方法。该方法使用了一种荧光甾醇——脱氢麦角固醇,以及一种化学猝灭剂——三硝基苯磺酸。脱氢麦角固醇可作为甾醇的探针分子,原因如下:(a) 脱氢麦角固醇不含作为报告基团的庞大侧链。(b) 脱氢麦角固醇在结构上类似于胆固醇和去氢胆固醇,而去氢胆固醇是LM成纤维细胞合成的主要甾醇。(c) 脱氢麦角固醇与洋地黄皂苷、制霉菌素相互作用,并可作为胆固醇氧化酶的底物。(d) 二棕榈酰甘油磷酸胆碱的相变被脱氢麦角固醇完全消除。(e) LM成纤维细胞的天然甾醇——去氢胆固醇,被脱氢麦角固醇完全取代,而对LM细胞生长、细胞倍增时间、质膜(Na +,K +)-ATP酶和5'-核苷酸酶活性、微粒体NADPH依赖性细胞色素c还原酶活性以及线粒体琥珀酸依赖性细胞色素c还原酶活性均无影响。(f) 补充脱氢麦角固醇不会改变LM成纤维细胞的磷脂组成或甾醇/磷脂比率。三硝基苯磺酸处理的三硝基苯基甘氨酸或LM成纤维细胞或红细胞表面膜的三硝基苯基基团是脱氢麦角固醇荧光的优良猝灭剂。当猝灭剂仅存在于膜的细胞外侧时,小鼠极低密度脂蛋白、LM成纤维细胞质膜、红细胞表面膜以及大鼠红细胞膜中的荧光分别被猝灭95±3%、20±2%、75±4%和69±4%。当膜甾醇中脱氢麦角固醇的含量为1 - 85 mol/100 ml时,三硝基苯基残基可有效猝灭LM细胞质膜中20%的脱氢麦角固醇荧光。当质膜两侧都用三硝基苯基化时,超过95%的脱氢麦角固醇荧光被猝灭。此外,当LM细胞用脱氢麦角固醇、暴露的乳胶珠培养,并在非穿透条件下将内吞颗粒分离为吞噬体并用三硝基苯磺酸处理时,脱氢麦角固醇的荧光几乎被猝灭64%。从这些及其他结果我们推断,LM成纤维细胞质膜的内层富含脱氢麦角固醇。相比之下,红细胞膜中甾醇的分布表明其在外层单分子层中富集。