Ferrero M E, Ferrero E, Bernelli-Zazzera A
J Natl Cancer Inst. 1977 Mar;58(3):645-50. doi: 10.1093/jnci/58.3.645.
Ascites hepatoma cells grown in Wistar rats were incubated anaerobically in the absence of glucose or in the presence of both glucose and D(+)glucosamine, or monoiodoacetate, or NADH, which interfered with glycolysis at different steps and with different mechanisms: Under all these conditions the incorporation of amino acids into the proteins of hepatoma cells was severely reduced without any clear relationship to the degree of inhibition of glycolysis. The postmitochondrial supernatants showed defective incorporation only when obtained from cells incubated in the absence of glucose or in the presence of monolodoacetate; inhibition of glycolysis by glucosamine and NADH did not seem to affect the subcellular basis for protein synthesis. When present, the defect of the cell sap (monoiodoacetate and absence of glucose) and to disaggregation and reduced functional capacity of the polysomes (absence of glucose). The results suggested that the effects of the inhibition of glycolysis on protein synthesis and on the integrity of the protein-synthesizing machinery--which were primarily due to the depletion of the energy stores--might have been modified by the particular mechanism of action of the inhibitor and by the way low levels of ATP were reached in the cell.
在Wistar大鼠体内生长的腹水肝癌细胞,在无葡萄糖的情况下,或在同时存在葡萄糖和D(+)氨基葡萄糖、或碘乙酸、或NADH的情况下进行厌氧培养,这些物质在不同步骤以不同机制干扰糖酵解:在所有这些条件下,氨基酸掺入肝癌细胞蛋白质的过程均严重减少,且与糖酵解的抑制程度无明显关系。仅当线粒体后上清液取自无葡萄糖或存在碘乙酸培养的细胞时,才显示掺入缺陷;氨基葡萄糖和NADH对糖酵解的抑制似乎并未影响蛋白质合成的亚细胞基础。当存在时,细胞液的缺陷(碘乙酸和无葡萄糖)以及多核糖体的解聚和功能能力降低(无葡萄糖)。结果表明,糖酵解抑制对蛋白质合成和蛋白质合成机制完整性的影响——主要是由于能量储备的耗尽——可能已被抑制剂的特定作用机制以及细胞中低水平ATP的产生方式所改变。