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首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >Paradoxical effect of cytosine arabinoside on mouse leukemia cell line L1210 cells.
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Paradoxical effect of cytosine arabinoside on mouse leukemia cell line L1210 cells.

机译：阿糖胞苷对小鼠白血病细胞L1210细胞的反常作用。

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We investigated the effects of 1-beta-D-arabinofuranosylcytosine (ara-C) on the growth of murine leukemic L1210 cells, which were cultured with high (2.0 x 10(3) ng/ml), middle (100 ng/ml) and low doses (5.0 ng/ml) of ara-C. In the analysis by flow cytometry, high dose ara-C arrested the cell cycle in the G0/G1-phase. Middle and low doses ara-C induced a block in the S-phase, that was not completely blocked by the low dose. Analysis of DNA fragmentation revealed that ara-C dose-dependently induced apoptosis, which was only slightly induced by the low dose. We measured activities of cellular thymidylate synthase (TS) and thymidine kinase (TK) after 24-h culture. Low and middle doses, but not high dose ara-C markedly enhanced TS activity to 2.9- in low and 5.3-fold in middle doses ara-C, and TK activity to 1.3- in low and 2.2-fold in middle doses, respectively, compared with those of the control. The cells accumulated in the S-phase by 48-h culture with low dose ara-C and markedly proliferated compared to that of the control in ara-C-free medium. These results indicate that non-high dose ara-C enhances DNA-synthesizing enzyme activities in L1210 cells, and withdrawal of the non-high dose ara-C results in paradoxical cell proliferation. Thus, daily intramuscular injections with an insufficient dose of ara-C may induce cells into S-phase, resulting in the proliferation of leukemic cells.
机译：我们研究了1-β-D-阿拉伯呋喃糖基胞嘧啶（ara-C）对高（2.0 x 10（3）ng / ml）中（100 ng / ml）培养的鼠白血病L1210细胞生长的影响和低剂量（5.0 ng / ml）的ara-C。在流式细胞仪分析中，高剂量的ara-C使细胞周期停滞在G0 / G1期。中低剂量ara-C引起S期阻滞，低剂量并未完全阻滞。 DNA片段分析显示，ara-C剂量依赖性地诱导凋亡，而低剂量仅轻微诱导其凋亡。我们测量了24小时培养后细胞胸苷酸合酶（TS）和胸苷激酶（TK）的活性。低剂量和中剂量但不是高剂量ara-C分别将TS活性分别降低到中等剂量ara-C的2.9-和5.3倍，而TK活性分别降低了中剂量的1.3-和2.2-倍。与对照组相比。在低剂量ara-C下通过48小时培养在S期中积累的细胞与在无ara-C的培养基中的对照细胞相比明显增殖。这些结果表明，非高剂量的ara-C增强了L1210细胞中的DNA合成酶活性，而撤出非高剂量的ara-C则导致了自相矛盾的细胞增殖。因此，每天肌内注射剂量不足的ara-C可能会诱导细胞进入S期，导致白血病细胞增殖。

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