Takagi M, Taki Y, Sakane T, Nadai T, Sezaki H, Oku N, Yamashita S
Faculty of Pharmaceutical Sciences, Setsunan University, Nagaotoge-cho, Hirakata, Osaka 573-01, Japan.
J Pharmacol Exp Ther. 1998 Jun;285(3):1175-80.
Transport of several monocarboxylic acids across the lipid bilayer was examined in liposomes consisting of egg yolk phosphatidylcholine and cholesterol. In the presence of inward proton gradient, salicylic acid (SA) was taken up rapidly by liposomes showing overshoot, saturation and competitive inhibition phenomena. These carrier-mediated like profiles of SA uptake can be explained by assuming a very high permeability through the liposomal membrane of protonated SA. Protonated SA in the extraliposomal solution (pH 5.8) was taken up by liposomes rapidly, followed by a redissociation to anion according to the intraliposomal pH (pH 7.5). The concentration gradient of protonated SA across the liposomal membrane is maintained until the intraliposomal pH decreased to the extraliposomal level, which facilitates the uptake of SA into liposomes. The permeability of the lipid bilayer to several compounds was estimated from the inhibitory effects of those compounds on SA uptake by liposomes. Good linear relationships were observed between their inhibitory effects on the liposomal uptake of SA and the permeability of the intestinal membrane to them determined both in vivo and in vitro. These results clearly indicate that the carrier-independent transport mechanism of monocarboxylic acids observed in liposomes significantly contributes to their absorption from the intestinal tract under physiological conditions.
在由蛋黄卵磷脂和胆固醇组成的脂质体中,研究了几种一元羧酸跨脂质双层的转运情况。在存在内向质子梯度的情况下,水杨酸(SA)被脂质体快速摄取,呈现出过冲、饱和和竞争性抑制现象。SA摄取的这些类似载体介导的特征可以通过假设质子化SA穿过脂质体膜具有非常高的渗透性来解释。脂质体外溶液(pH 5.8)中的质子化SA被脂质体快速摄取,随后根据脂质体内pH(pH 7.5)重新解离为阴离子。质子化SA跨脂质体膜的浓度梯度得以维持,直到脂质体内pH降至脂质体外水平,这促进了SA进入脂质体。根据这些化合物对脂质体摄取SA的抑制作用,估算了脂质双层对几种化合物的渗透性。观察到它们对脂质体摄取SA的抑制作用与在体内和体外测定的肠道膜对它们的渗透性之间存在良好的线性关系。这些结果清楚地表明,在脂质体中观察到的一元羧酸的非载体依赖性转运机制在生理条件下对它们从肠道的吸收有显著贡献。