Complete mapping of crystallization pathways during cholesterol precipitation from model bile: influence of physical-chemical variables of pathophysiologic relevance and identification of a stable liquid crystalline state in cold, dilute and hydrophilic b
Complete mapping of crystallization pathways during cholesterol precipitation from model bile: influence of physical-chemical variables of pathophysiologic relevance and identification of a stable liquid crystalline state in cold, dilute and hydrophilic b
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发表时间：
1996-03
影响因子：
6.5
通讯作者：
D. Q. Wang;M. Carey
中科院分区：
文献类型：
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作者：
D. Q. Wang;M. Carey
使用互补的物理化学技术，我们定义了五种不同的结晶途径作为时间（30天）和增加卵磷脂（蛋黄）含量的函数在病理生理相关模型胆汁过饱和（胆固醇饱和指数，1.2 - 2.7）稀释约等于29 g/dl的胆汁盐-卵磷脂-胆固醇胶束溶液。如通过准弹性光散射光谱所证明的，过饱和预示着由单层囊泡的外观。在卵磷脂含量最低时，首先出现具有与无水胆固醇一致的习性和密度（d 1.030 g/mL）的弧形晶体，并通过螺旋和管状晶体演化为板状胆固醇一水合物晶体（d 1.045 g/mL）。卵磷脂含量较高时，胆固醇一水合物晶体出现的时间早于ARC和其他过渡晶体。具有典型的生理卵磷脂含量，早期液晶（d 1.020 g/mL）其次是胆固醇一水合物晶体和随后出现的弧和其他中间晶体。随着卵磷脂含量的增加，液晶之后仅是胆固醇一水合物晶体，并且在最高卵磷脂摩尔分数下，出现不产生固体晶体的液晶。添加钙增加固体晶体数与其浓度（5 - 20 mM）成比例，但不影响外观时间，结晶途径，或胶束胆固醇溶解度。降低温度（37度-> 4摄氏度），总脂质浓度（7.3 -> 2.4 g/dL）和胆盐疏水性（3 α，12 α-> 3 α，7 α，12 α-> 3 α，7 β羟基化牛磺酸缀合物）逐渐将所有结晶途径转移到较低的卵磷脂含量，延迟结晶，和降低的胶束胆固醇溶解度。在结晶过程中，特别是当平衡时液晶共存时，胆油中卵磷脂的含量显著降低。这项系统的研究提供了一个框架，了解胆固醇结晶在人类和动物胆汁，并检查影响相分离动力学的因素。
Using complementary physical-chemical techniques we defined five different crystallization pathways as functions of time (30 days) and increasing lecithin (egg yolk) content in pathophysiologically relevant model biles super-saturated (cholesterol saturation indices, 1.2 - 2.7) by dilution of approximately equal to 29 g/dl bile salt-lecithin-cholesterol micellar solutions. As evidenced by quasi-elastic light-scattering spectroscopy, supersaturation was heralded by the appearance of unilamellar vesicles. With the lowest lecithin contents, arc-like crystals with habit and density (d 1.030 g/mL) consistent with anhydrous cholesterol appeared first and evolved via helical and tubular crystals to form plate-like cholesterol monohydrate crystals (d 1.045 g/mL). With higher lecithin fractions, cholesterol monohydrate crystals appeared earlier than arc and other transitional crystals. With typical physiological lecithin contents, early liquid crystals (d 1.020 g/mL) were followed by cholesterol monohydrate crystals and subsequent appearances of arc and other intermediate crystals. With higher lecithin contents, liquid crystals were followed by cholesterol monohydrate crystals only, and at the highest lecithin mole fractions, liquid crystals appeared that did not generate solid crystals. Added calcium increased solid crystal number in proportion to its concentration (5 - 20 mM) but did not influence appearance times, crystallization pathways, or micellar cholesterol solubilities. Decreases in temperature (37 degrees --> 4 degrees C), total lipid concentration (7.3 --> 2.4 g/dL), and bile salt hydrophobicity (3 alpha, 12 alpha --> 3 alpha, 7 alpha, 12 alpha --> 3 alpha, 7 beta hydroxylated taurine conjugates) progressively shifted all crystallization pathways to lower lecithin contents, retarded crystallization, and decreased micellar cholesterol solubilities. The lecithin content of mother biles decreased markedly during crystallization especially where liquid crystals were a coexisting phase at equilibrium. This systematic study provides a framework for understanding cholesterol crystallization in human and animal biles and for examining factors that influence the kinetics of phase separation.