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秋水仙碱(秋水仙酰胺)对小鼠肉瘤180肿瘤的作用。

Action of demecolcine (colcemid) in the murine sarcoma 180 tumor.

作者信息

Nomura T, Plager J E

出版信息

Cancer Treat Rep. 1981 Mar-Apr;65(3-4):283-90.

PMID:7237451
Abstract

Iv infusions of demecolcine (Colcemid) were established in mice bearing the Sarcoma 180 tumor. During demecolcine infusion at a rate of 6 microgram/hr, the tumor labeling index following 3H-thymidine administration and the mean grain count per labeled cell did not differ significantly from control values. Cells in anaphase and telophase disappeared from the tumor sections, and the net number of cells in the earlier stages of mitosis increased for 20 hrs. The rate of mitotic accumulation during the initial 8 hrs of demecolcine infusion was about one third of what would be expected from the known cell cycle values for this tumor. This reduced rate of accumulation does not appear to result from death of mitotic cells, escape of cells from metaphase blockade, or S-phase arrest secondary to inhibition of DNA synthesis; it is suggested that the reduced accumulation rate is secondary to demecolcine damage to interphase cells. Tumor cells that have been gathered by 4-hr demecolcine infusions may be released in synchronous fashion following the end of the infusion. A small proportion of these cells will recycle synchronously during the following mitotic period.

摘要

对携带肉瘤180肿瘤的小鼠进行了秋水仙碱(秋水仙酰胺)静脉输注。以6微克/小时的速率输注秋水仙碱期间,给予3H-胸腺嘧啶核苷后肿瘤标记指数以及每个标记细胞的平均颗粒计数与对照值相比无显著差异。肿瘤切片中处于后期和末期的细胞消失,有丝分裂前期阶段的细胞净数量在20小时内增加。秋水仙碱输注最初8小时内有丝分裂积累速率约为根据该肿瘤已知细胞周期值预期速率的三分之一。这种积累速率降低似乎并非由于有丝分裂细胞死亡、细胞从中期阻滞中逃脱或DNA合成受抑制继发的S期停滞所致;提示积累速率降低是秋水仙碱对间期细胞造成损伤的继发结果。经4小时秋水仙碱输注收集的肿瘤细胞在输注结束后可能会以同步方式释放。这些细胞中的一小部分将在随后的有丝分裂期同步循环。

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