Kaledin V I, Nikolin V P, Baimak T Yu, Galyamova M R, Popova N A, Andreeva E M
Institute of Cytology and Genetics, Siberian Branch of Russian Academy of Sciences, Novosibirsk.
Bull Exp Biol Med. 2003 Mar;135(3):289-92. doi: 10.1023/a:1024101518194.
Antitumor effect of cyclophosphamide on LS and P388 tumors is realized via apoptosis and on HA-1 and Krebs-2 tumors resistant to apoptosis via necrosis of tumor cells. Phenobarbital induction of cyclophosphamide-metabolizing enzymes decreases and cimetidine inhibition potentiates the effect of cyclophosphamide on LS and P388 cells and does not modulate the effect on HA-1 and Krebs-2 cells. Presumably, apoptosis and necrosis of tumor cell are induced by different cyclophosphamide metabolites.
环磷酰胺对LS和P388肿瘤的抗肿瘤作用是通过细胞凋亡实现的,而对HA - 1和Krebs - 2等抗细胞凋亡肿瘤则是通过肿瘤细胞坏死实现的。苯巴比妥诱导的环磷酰胺代谢酶减少,西咪替丁抑制则增强环磷酰胺对LS和P388细胞的作用,且不调节对HA - 1和Krebs - 2细胞的作用。据推测,肿瘤细胞的凋亡和坏死是由不同的环磷酰胺代谢产物诱导的。