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首页> 美国卫生研究院文献>British Journal of Cancer >Effects of cycloheximide on B-chronic lymphocytic leukaemic and normal lymphocytes in vitro: induction of apoptosis.
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Effects of cycloheximide on B-chronic lymphocytic leukaemic and normal lymphocytes in vitro: induction of apoptosis.

机译：环己酰亚胺对体外B慢性淋巴细胞白血病和正常淋巴细胞的影响：诱导凋亡。

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A number of reports indicate that protein synthesis is a requirement for the occurrence of apoptosis. In this study, the effect of the protein synthesis inhibitor cycloheximide (CHM) on spontaneous apoptosis of B-chronic lymphocytic leukaemia (B-CLL) cells, previously shown to occur when they are cultured in RPMI-1640 medium with autologous or heterologous serum, was examined. No definite inhibition of apoptosis was observed. Indeed, CHM-treatment augmented apoptosis in the B-CLL cultures and also induced apoptosis of cultured normal peripheral blood lymphocytes. Augmentation was dose-dependent for B-CLL cells over the concentration range 10(-6) M (0.28 micrograms ml-1) to 10(-2) M (2800 micrograms ml-1), resulting in 9% to 98% apoptosis respectively by 24 h of culture (r = 0.619, P = 0.0008). Normal lymphocytes were affected by CHM over the range 10(-4) M to 10(-2) M, resulting in 7% to 74% apoptosis respectively (r = 0.794, P = 0.0001). Inhibition of protein synthesis in these cells by CHM was virtually complete at a concentration of 10(-3) M. The findings are in accord with some recent reports indicating that suppression of protein synthesis by CHM does not inhibit apoptosis in all circumstances. They also illustrate the marked susceptibility of B-CLL cells, compared with normal lymphocytes, to the induction of apoptosis by this drug. The manner in which CHM triggers apoptosis of some cell types is at present uncertain.
机译：许多报告表明蛋白质合成是发生细胞凋亡的必要条件。在这项研究中，蛋白质合成抑制剂环己酰亚胺（CHM）对B慢性淋巴细胞性白血病（B-CLL）细胞自发凋亡的影响，先前显示是在带有自体或异源血清的RPMI-1640培养基中培养它们后产生的，被检查了。没有观察到明确的凋亡抑制作用。实际上，CHM处理增加了B-CLL培养物中的细胞凋亡，并且还诱导了培养的正常外周血淋巴细胞的细胞凋亡。 B-CLL细胞在10（-6）M（0.28微克ml-1）至10（-2）M（2800微克ml-1）浓度范围内的增强剂量依赖性，导致9％至98％的细胞凋亡分别培养24小时（r = 0.619，P = 0.0008）。正常淋巴细胞在10（-4）M至10（-2）M范围内受CHM影响，分别导致7％至74％的凋亡（r = 0.794，P = 0.0001）。在浓度为10（-3）M的条件下，CHM对这些细胞中蛋白质合成的抑制作用实际上已完全完成。该发现与一些最新报告相符，这些报道表明，CHM抑制蛋白质合成并不能在所有情况下均抑制细胞凋亡。他们还说明了与正常淋巴细胞相比，B-CLL细胞对这种药物诱导的细胞凋亡具有明显的敏感性。目前尚不清楚CHM触发某些细胞类型凋亡的方式。

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