Parekh H K, Chitnis M P
Cellular Chemotherapy Unit, Tata Memorial Centre, Parel, Bombay, India.
Oncology. 1990;47(6):501-7. doi: 10.1159/000226880.
Differential effects of adriamycin cytotoxicity and its cellular uptake were assessed in murine tumor models utilising adriamycin alone and in combination with nontoxic concentrations of nonionic polyoxyethylated lauryl ether surfactants Brij 30 and Brij 35. Parental P388 murine leukemia cell line sensitive to adriamycin, subline of P388 murine leukemia resistant to adriamycin, sarcoma-180 and Ehrlich ascites tumor were employed in this study. The results indicate an enhanced DNA biosynthesis inhibition by adriamycin when used in combination with Brij 30 or Brij 35 in all the murine tumor models. The increase in adriamycin cytotoxicity was due to an increased accumulation of adriamycin observed in the tumor models used. The present investigation demonstrates the necessity of utilising surface-active drug-response modulators to enhance the cytotoxicity of anticancer drugs and circumvent drug resistance.
在小鼠肿瘤模型中，评估了阿霉素细胞毒性及其细胞摄取的差异效应，分别单独使用阿霉素以及将其与无毒浓度的非离子聚氧乙烯化月桂醚表面活性剂Brij 30和Brij 35联合使用。本研究采用了对阿霉素敏感的亲本P388小鼠白血病细胞系、对阿霉素耐药的P388小鼠白血病亚系、肉瘤-180和艾氏腹水瘤。结果表明，在所有小鼠肿瘤模型中，阿霉素与Brij 30或Brij 35联合使用时，对DNA生物合成的抑制作用增强。阿霉素细胞毒性的增加是由于在所使用的肿瘤模型中观察到阿霉素的积累增加。本研究表明，利用表面活性药物反应调节剂来增强抗癌药物的细胞毒性并规避耐药性是必要的。
