Moore E W
Hepatology. 1984 Sep-Oct;4(5 Suppl):228S-243S.
Calcium is present in all pigment gallstones as a salt of one or more of the anions in bile which are most readily precipitable by calcium: (i) carbonate; (ii) bilirubinate; (iii) phosphate, and (iv) "palmitate". We term these "calcium-sensitive" anions. In addition, since cholesterol stones have been found to contain pigment stone centers, we postulate that calcium precipitation in bile is a critical event in the initiation of cholesterol gallstones, so that the latter should be considered a two-stage process: (i) precipitation of calcium salts to form a nidus, and (ii) precipitation of cholesterol from its supersaturated state on this nidus. Any measure which will reduce free [Ca++] in bile will reduce calcium lithogenicity; possible ways to reduce [Ca++] in bile are presented. One way is to increase Ca++ binding by normal biliary constituents; we have recently pointed out that bile salts are important buffers for Ca++ in bile by virtue of binding to both free and micellar bile salts. Here, we consider some of our Ca++ electrode studies of taurocholate, glycocholate, serum albumin, and simple molecules having terminal carboxyl (CO0-) or sulfonic (SO-3) ions. A brief history of the development of the Ca++ electrode is given, along with theoretical considerations of ionic activities and techniques of electrode measurements. From the various studies, a unifying hypothesis is proposed for the structural requirements of Ca++-binding to proteins (albumin) and free monomeric bile salts. For proteins, unconjugated bile salts and glycine-conjugated bile salts, it is proposed that Ca++ binding involves a reversible ion-exchange "site" in which a Ca++ ion is interposed between carboxyl (CO0-) and hydroxyl (OH) groups. For taurine-conjugated bile salts, this "site" is proposed to involve the interposition of a Ca++ ion between the side-chain SO-3 and cholanic ring OH groups. These studies are a first step toward modulation of Ca++ activity in bile.
（i）碳酸盐；（ii）胆红素盐；（iii）磷酸盐，以及（iv）“棕榈酸盐”。我们将这些称为“钙敏感”阴离子。此外，由于已发现胆固醇结石含有色素结石核心，我们推测胆汁中的钙沉淀是胆固醇胆结石形成起始阶段的关键事件，因此后者应被视为一个两阶段过程：（i）钙盐沉淀形成核心，以及（ii）胆固醇从其过饱和状态在该核心上沉淀。任何降低胆汁中游离[Ca++]的措施都会降低钙的致石性；文中介绍了降低胆汁中[Ca++]的可能方法。一种方法是增加正常胆汁成分对Ca++的结合；我们最近指出，胆汁盐通过与游离和胶态胆汁盐结合，是胆汁中Ca++的重要缓冲剂。在此，我们考虑一些我们用Ca++电极对牛磺胆酸盐、甘氨胆酸盐、血清白蛋白以及具有末端羧基（COO-）或磺酸基（SO3-）离子的简单分子所做的研究。文中给出了Ca++电极发展的简要历史，以及离子活度的理论考量和电极测量技术。从各种研究中，针对Ca++与蛋白质（白蛋白）和游离单体胆汁盐结合的结构要求提出了一个统一的假说。对于蛋白质、未结合胆汁盐和甘氨酸结合胆汁盐，提出Ca++结合涉及一个可逆的离子交换“位点”，其中一个Ca++离子介于羧基（COO-）和羟基（OH）基团之间。对于牛磺酸结合胆汁盐，该“位点”被认为涉及一个Ca++离子介于侧链SO3-和胆烷环OH基团之间。这些研究是调节胆汁中Ca++活性的第一步。
