Günther T, Averdunk R
J Clin Chem Clin Biochem. 1976 Jul;14(7):365-71.
X-537A, an ionophore for divalent cations, causes a rapid replacement of extracellular Na+ by intracellular K+ in Yoshida ascites tumour cells. The loss of K+ is prevented by high extracellular concentrations of K+. In incubation solutions containing Ca2+, the Ca2+ content of the tumour cells increases in the presence of X-537A, but the Mg2+ content is not affected. The intracellular level of cyclic AMP is also increased. In all the incubation media used, the presence of X-537A resulted in a decrease in biosynthesis in the order RNA greater than DNA greater than protein, at constant ATP concentration. The observed changes in the content of electrolytes and cyclic AMP, and on the metabolism of DNA, RNA and protein in Yoshida ascites tumour cells in response to X-537A, correspond to those observed during Mg deficiency in these cells. These changes are caused by changes in the intracellular concentrations of Ca2+ and/or K+.
X-537A是一种二价阳离子离子载体,可使吉田腹水瘤细胞中的细胞外Na+迅速被细胞内K+取代。高细胞外K+浓度可防止K+流失。在含有Ca2+的培养液中,X-537A存在时肿瘤细胞的Ca2+含量增加,但Mg2+含量不受影响。细胞内的环磷酸腺苷(cAMP)水平也会升高。在所有使用的培养液中,在ATP浓度恒定的情况下,X-537A的存在导致生物合成减少,减少顺序为RNA>DNA>蛋白质。吉田腹水瘤细胞中观察到的电解质和环磷酸腺苷含量的变化,以及对X-537A的DNA、RNA和蛋白质代谢的变化,与这些细胞中镁缺乏时观察到的变化一致。这些变化是由细胞内Ca2+和/或K+浓度的变化引起的。