Trentesaux C, Laplace B, Madoulet C, Rebel G, Jardillier J C
Anticancer Res. 1987 Mar-Apr;7(2):187-92.
The antitumor agent Adriamycin (ADM) increases the sialic acid content of K 562 cell plasma membrane glycoconjugates. Total and neuraminidase-sensitive sialic acid are enhanced 3 to 4 times when expressed per 10(6) cells. This fact is a consequence of an increase in cell surface and in plasma membrane sialic acid density. Protein-bound and lipid-bound sialic acid are increased in the same way and exhibit the same ratio 90/10. After external radiolabelling by periodide-borotritide and neuraminidase-galactose oxidase-borotritide treatment, only some quantitative changes can be observed. Fractionation of gangliosides by thin layer chromatography gives the same results. Further experiments lead to the following conclusions: the hypersialylation cannot be explained by a G2-block in the cell cycle induced by ADM; it is not a consequence of a differentiation process; it is not observed in a population of adriamycin-resistant K 562 cells and can therefore be considered as a metabolic event linked to the cytotoxic activity of ADM.
抗肿瘤药物阿霉素（ADM）可增加K 562细胞质膜糖缀合物的唾液酸含量。以每10⁶个细胞计算，总唾液酸和对神经氨酸酶敏感的唾液酸增加3至4倍。这一事实是细胞表面和质膜唾液酸密度增加的结果。与蛋白质结合和与脂质结合的唾液酸以相同方式增加，且呈现相同的90/10比例。经过碘硼化三氢外部放射性标记以及神经氨酸酶 - 半乳糖氧化酶 - 硼化三氢处理后，仅能观察到一些定量变化。通过薄层色谱法对神经节苷脂进行分级分离得到相同结果。进一步实验得出以下结论：高唾液酸化不能用ADM诱导的细胞周期G2期阻滞来解释；它不是分化过程的结果；在阿霉素耐药的K 562细胞群体中未观察到这种现象，因此可被视为与ADM细胞毒性活性相关的代谢事件。
