Denis-Gay M, Petit J M, Ratinaud M H
Institut de Biotechnologie, Faculté des Sciences, Limoges, France.
Anticancer Res. 1995 Jan-Feb;15(1):121-6.
The ability of the P-glycoprotein to efflux rhodamine 123 and adriamycin was evaluated using adriamycin-sensitive and -resistant human leukemia K562 cells. We observed that low temperature or verapamil (a P-glycoprotein blocker) inhibited adriamycin efflux in multidrug resistant cells. In the same conditions, resistant K562 cells did not significantly retain rhodamine 123. This dye was located in the cytoplasm of resistant cells and did not display spectral properties characteristic of stacked rhodamine 123 molecules in mitochondria of sensitive K562 cells. Thus, in adriamycin-resistant K562 cells, the rhodamine efflux may be due to P-glycoprotein activity and also to a nonspecific targeting of dye in resistant K562 cells.
利用对阿霉素敏感和耐药的人白血病K562细胞,评估P-糖蛋白对罗丹明123和阿霉素的外排能力。我们观察到低温或维拉帕米(一种P-糖蛋白阻滞剂)可抑制多药耐药细胞中的阿霉素外排。在相同条件下,耐药的K562细胞并未显著保留罗丹明123。这种染料位于耐药细胞的细胞质中,并未表现出敏感K562细胞线粒体中罗丹明123分子堆积的光谱特性。因此,在阿霉素耐药的K562细胞中,罗丹明外排可能归因于P-糖蛋白活性,也可能归因于耐药K562细胞中染料的非特异性靶向作用。