<原著>分離ラット細胆管側肝細胞膜における抱合型ビリルビンの輸送機構について

概要

論文の詳細を見る
To elucidate the mechanism of bilirubin diglucuronide (BDG) excretion through the hepatocyte canalicular membrane, BDG transport was studied in isolated liver canalicular membrane vesicles by a rapid filtration method. BDG transport was not dependent on Na^+. BDG uptake was saturable (apparent Km for BDG=75μM and V_<MAX>=0.42n mol/mg protein×20s at 37℃) and was inhibited by BSP, but the inhibition by taurocholate was very small. By preincubation with unlabelled BDG, trans-stimulation of BDG transport could also be demonstrated. When the electrical potential difference across the membrane was altered by anion replacement, a more positive intravesicular potential stimulated, and a more negative potential inhibited BDG transport. Valinomycin-induced K^+ diffusion potential also enhanced BDG uptake. However, the use of inwardly directed inorganic ion gradients resulted in enhancement of [^3H]-BDG transport when Cl- was used. These findings provide direct evidence for the presence of a carrier mediated, sodium-independent and potential-sensitive BDG transport in rat liver canalicular membrane. In intact hepatocytes, the electrolical potential difference across the canalicylar membrane (about-30〜-35mV) may provide the driving force BDG excretion.
近畿大学の論文
1991-06-25