Tsukazaki Masashi, Satsu Hideo, Mori Akira, Sugita-Konishi Yoshiko, Shimizu Makoto
Department of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-8657, Japan.
Biochem Biophys Res Commun. 2004 Mar 19;315(4):991-7. doi: 10.1016/j.bbrc.2004.01.147.
The effect of tributyltin (TBT) on human intestinal epithelial cell functions was investigated by using human intestinal Caco-2 cell monolayers. We paid particular attention to the effect of TBT on two barrier functions: the tight junction as a physical barrier and MDR1/P-glycoprotein as a biological barrier. A loss of monolayer integrity was apparent from the TBT treatment and the paracellular permeability was increased by TBT. On the other hand, the activity of P-glycoprotein, which was examined by measuring the accumulation of Rhodamine-123 and daunomycin, was increased by prolonged TBT treatment in a concentration-dependent manner (1-100 nM). Furthermore, it was clarified by Western and Northern blots that this increase was accompanied by the increased expression of MDR1 mRNA and protein. The activation of a multidrug resistance transporter P-glycoprotein by TBT would cause a disorder of the human intestines by changing the drug pharmacokinetics.
通过使用人肠道Caco-2细胞单层来研究三丁基锡(TBT)对人肠道上皮细胞功能的影响。我们特别关注TBT对两种屏障功能的影响:作为物理屏障的紧密连接和作为生物屏障的MDR1/ P-糖蛋白。TBT处理后单层完整性明显丧失,并且TBT增加了细胞旁通透性。另一方面,通过测量罗丹明-123和柔红霉素的积累来检测的P-糖蛋白活性,在延长的TBT处理(1-100 nM)中以浓度依赖性方式增加。此外,通过蛋白质印迹法和Northern印迹法表明,这种增加伴随着MDR1 mRNA和蛋白质表达的增加。TBT对多药耐药转运蛋白P-糖蛋白的激活会通过改变药物药代动力学而导致人体肠道紊乱。