The aim of our research reported in this paper is to mimic and understand gallstone formation. The precipitation of calcium carbonate by reacting CaCl2 with NaHCO3 in model bile containing 68.6 mol % of taurocholate. 22.9 mol % of lecithin, and 8.5 mol % of cholesterol with a total lipid (taurocholate + lecithin + cholesterol) concentration of 29.2 g/dL was followed by a calcium ion meter. The 36-h old biomimetic stones collected were analyzed for cholesterol. content (CC) by thermal gravimetric analysis, for vaterite-to-calcite ratio (Rv-c) by powder X-ray diffraction, and for morphology by scanning electron microscopy. The stability of model bile was also disturbed with seeds of anhydrous cholesterol, cholesterol monohydrate, lysozyme, sodium taurocholate, and CaCO3 crystals. We found that lecithin itself was capable of inducing the formation of vaterite or slowing down the vaterite-to-calcite transformation probably through its positively charged choline moiety to produce high Ca2+ ion concentrations near the Vesicular Surface and to stabilize the negatively charged [00 (1) over bar] plane of vaterite nanocrystals. The mixture of vaterite and calcite nanocrystals was then aggregated and aligned under the direction of the crystal surface adsorbed lecithin molecules to form mesocrystals. Disturbing the stability of the microscopic structure of the complex lipid system could in principle release the Vesicular adsorbed Ca2+ ions and the solubilized cholesterol so that calcium carbonate and cholesterol microcrystals Could be precipitated out even when the cholesterol saturation index (CSI) < 1. We proposed that this was an autocatalytic cycle because the newly precipitated calcium carbonate and cholesterol microcrystals could then serve as seeds to further worsen the stability of the complex lipid system. Besides the microcrystals of calcium carbonate and cholesterol, other biliary components such as Ca2+ and HCO3- ions, bile salts, and proteins were also capable of destabilizing the complex lipid system.
