Huang R N, Lee T C
Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, R.O.C.
Toxicol Appl Pharmacol. 1996 Nov;141(1):17-22. doi: 10.1006/taap.1996.0255.
We have previously demonstrated that arsenite-resistant SA7 cells can extrude arsenite more effectively and completely than their parental Chinese hamster ovary cells. Our present results show that arsenite efflux from SA7 cells is inhibited by chemosensitizing agents to multidrug resistant-associated protein: verapamil and cyclosporin A and by glutathione-depleting agents: dinitrofluorobenzene and diethyl maleate. These results suggest that arsenite extrusion in SA7 cells may be mediated by a GSH-dependent and verapamil- and cyclosporin A-sensitive membrane transport system. Since arsenite extrusion was found dose-dependently inhibited by energy poison [potassium cyanide (KCN)] and an ATPase inhibitor (sodium vanadate), ATP is apparently required for arsenite extrusion in SA7 cells.
我们之前已经证明，抗亚砷酸盐的SA7细胞比亚砷酸盐敏感的亲本中国仓鼠卵巢细胞能更有效、更彻底地排出亚砷酸盐。我们目前的结果表明，SA7细胞中的亚砷酸盐流出受到多药耐药相关蛋白的化学增敏剂（维拉帕米和环孢菌素A）以及谷胱甘肽消耗剂（二硝基氟苯和马来酸二乙酯）的抑制。这些结果表明，SA7细胞中的亚砷酸盐排出可能由一种依赖谷胱甘肽且对维拉帕米和环孢菌素A敏感的膜转运系统介导。由于发现亚砷酸盐排出受到能量毒物[氰化钾（KCN）]和ATP酶抑制剂（钒酸钠）的剂量依赖性抑制，因此SA7细胞排出亚砷酸盐显然需要ATP。
