Department of Pharmaceutical Sciences, University of Michigan College of Pharmacy, 428 Church Street, Ann Arbor, Michigan 48109, USA.
Mol Pharm. 2010 Apr 5;7(2):456-67. doi: 10.1021/mp9001969.
A biophysical, computational model of cell pharmacokinetics (1CellPK) is being developed to enable prediction of the intracellular accumulation and transcellular transport properties of small molecules using their calculated physicochemical properties as input. To test if 1CellPK can generate accurate, quantitative hypotheses and guide experimental analysis of the transcellular transport kinetics of small molecules, epithelial cells were grown on impermeable polyester membranes with cylindrical pores and chloroquine (CQ) was used as a transport probe. The effect of the number of pores and their diameter on transcellular transport of CQ was measured in apical-to-basolateral or basolateral-to-apical directions, at pH 7.4 and 6.5 in the donor compartment. Experimental and simulation results were consistent with a phospholipid bilayer-limited, passive diffusion transport mechanism. In experiments and 1CellPK simulations, intracellular CQ mass and the net rate of mass transport varied <2-fold although total pore area per cell varied >10-fold, so by normalizing the net rate of mass transport by the pore area available for transport, cell permeability on 3 mum pore diameter membranes was more than an order of magnitude less than on 0.4 mum pore diameter membranes. The results of simulations of transcellular transport were accurate for the first four hours of drug exposure, but those of CQ mass accumulation were accurate only for the first five minutes. Upon prolonged incubation, changes in cellular parameters such as lysosome pH rise, lysosome volume expansion, and nuclear shrinkage were associated with excess CQ accumulation. Based on the simulations, lysosome volume expansion alone can partly account for the measured, total intracellular CQ mass increase, while adding the intracellular binding of the protonated, ionized forms of CQ (as reflected in the measured partition coefficient of CQ in detergent-permeabilized cells at physiological pH) can further improve the intracellular CQ mass accumulation prediction.
正在开发一种细胞药代动力学的生物物理、计算模型(1CellPK),以便能够使用小分子的计算物理化学特性作为输入来预测其细胞内积累和跨细胞转运特性。为了测试 1CellPK 是否可以生成准确的、定量的假说并指导小分子跨细胞转运动力学的实验分析,将上皮细胞种植在具有圆柱形孔的不可渗透聚酯膜上,并使用氯喹(CQ)作为转运探针。在供体室中 pH 值为 7.4 和 6.5 时,以 apical-to-basolateral 或 basolateral-to-apical 方向测量了孔的数量及其直径对 CQ 跨细胞转运的影响。实验和模拟结果与磷脂双层限制的、被动扩散转运机制一致。在实验和 1CellPK 模拟中,尽管细胞内 CQ 质量和净质量转运率变化<2 倍,但每个细胞的总孔面积变化>10 倍,因此通过将净质量转运率除以可用的转运孔面积进行归一化,3 µm 孔径膜上的细胞通透性比 0.4 µm 孔径膜上的通透性低一个数量级以上。在药物暴露的前四个小时,跨细胞转运的模拟结果是准确的,但 CQ 积累的模拟结果仅在最初的五分钟内是准确的。随着孵育时间的延长,细胞参数的变化,如溶酶体 pH 值升高、溶酶体体积膨胀和核收缩,与过量 CQ 积累有关。基于模拟结果,仅溶酶体体积膨胀就可以部分解释所测量的细胞内 CQ 总量增加,而加入 CQ 的质子化、离子化形式的细胞内结合(如在生理 pH 值下用去污剂通透化细胞测量的 CQ 分配系数所反映的)可以进一步提高细胞内 CQ 质量积累的预测。