Benestad H B, Heikkilä R
Blut. 1986 Nov;53(5):371-7. doi: 10.1007/BF00321099.
A new way of assessing the significance of intracellular signals that may regulate cellular proliferation, would be to analyze possible 'second messengers' when proliferation is slowed down, rather than stimulated. Therefore, we examined proliferating mononuclear blood cells from leukaemic patients which had been exposed to an inhibitory ox leucocyte extract. The extract decreased 3H-thymidine incorporation in leukaemic cells in short-term cultures. The inhibition was not cell-line specific, but was nevertheless non-toxic and not due to endotoxin. The K+ flux into the leukaemic cells was assessed with 86Rb+, a K+ analogue. An inverse relationship was found between 86Rb+ uptake and 3H-thymidine incorporation. The increased 86Rb+ influx was probably due to leakage or exchange mechanisms other than the Na+/K+ membrane pump, as suggested by ouabain inhibition experiments. However, the long lag time (greater than 45 min) between addition of inhibitor and a marked increase in 86Rb+ uptake does not support a role for the K+ flux as an early mediator of the inhibitory signal.
评估可能调节细胞增殖的细胞内信号重要性的一种新方法，是在增殖减缓而非受到刺激时分析可能的“第二信使”。因此，我们检测了来自白血病患者的增殖性单核血细胞，这些细胞已暴露于一种抑制性牛白细胞提取物中。该提取物在短期培养中降低了白血病细胞中3H-胸腺嘧啶核苷的掺入。这种抑制作用不是细胞系特异性的，但无毒且不是由内毒素引起的。用86Rb +（一种钾离子类似物）评估钾离子流入白血病细胞的情况。发现86Rb +摄取与3H-胸腺嘧啶核苷掺入之间呈负相关。哇巴因抑制实验表明，86Rb +流入增加可能是由于除钠钾膜泵之外的泄漏或交换机制。然而，添加抑制剂与86Rb +摄取显著增加之间的长延迟时间（大于45分钟）不支持钾离子通量作为抑制信号的早期介质起作用。
