McGown A, Poppitt D G, Fox B W
Department of Experimental Chemotherapy, Paterson Institute for Cancer Research, Christie Hospital, Withington, Manchester, UK.
Br J Cancer. 1987 Dec;56(6):752-4. doi: 10.1038/bjc.1987.283.
Two P388 cell lines with acquired resistance to daunorubicin have been shown to exhibit cross-resistance to anthrapyrazolone (NSC 357885). The degree of cross-resistance observed in these cell lines (58 and 150 fold) is similar to those observed towards daunorubicin (34 and 142 fold). However the decreased drug accumulation observed for daunorubicin in the resistant cell lines (4-6 fold) is not observed for anthrapyrazolone. Similarly, verapamil can increase daunorubicin accumulation in resistant cells but has no effect on anthrapyrazolone accumulation. It is concluded that in contrast to daunorubicin, decreased anthrapyrazolone accumulation is not the resistance mechanism operative in daunorubicin resistant cell lines towards anthrapyrazolone.
已证明两种对柔红霉素产生获得性耐药的P388细胞系对蒽吡唑啉(NSC 357885)表现出交叉耐药性。在这些细胞系中观察到的交叉耐药程度(58倍和150倍)与对柔红霉素观察到的程度(34倍和142倍)相似。然而,在耐药细胞系中观察到柔红霉素的药物积累减少(4 - 6倍),而蒽吡唑啉未出现这种情况。同样,维拉帕米可增加耐药细胞中柔红霉素的积累,但对蒽吡唑啉的积累没有影响。得出的结论是,与柔红霉素不同,蒽吡唑啉积累减少不是柔红霉素耐药细胞系对蒽吡唑啉产生耐药的作用机制。