This paper investigates the redistribution of metabolic fluxes in the cell with altered activity of S-adenosylmethionine decarboxylase (SAMdc, EC: 4.1.1.50), the key enzyme of the polyamine cycle and the common target for antitumor therapy. To address these goals, a stoichiometric metabolic model was developed that includes five metabolic pathways: polyamine, methionine, methionine salvage cycles, folic acid cycle, and the pathway of glutathione and taurine synthesis. The model is based on 51 reactions involving 57 metabolites, 31 of which are internal metabolites. All calculations were performed using the method of Flux Balance Analysis. The outcome indicates that the inactivation of SAMdc results in a significant increase in fluxes through the methionine, the taurine and glutathione synthesis, and the folate cycles. Therefore, when using therapeutic agents inactivating SAMdc, it is necessary to consider the possibility of cellular tumor metabolism reprogramming. S-adenosylmethionine affects serine methylation and activates serine-dependent de novo ATP synthesis. Methionine-depleted cell becomes methionine-dependent, searching for new sources of methionine. Inactivation of SAMdc enhances the transformation of S-adenosylmethionine to homocysteine and then to methionine. It also intensifies the transsulfuration process activating the synthesis of glutathione and taurine.

本文研究了S-腺苷甲硫氨酸脱羧酶（SAMdc，EC：4.1.1.50），多胺循环的关键酶和抗肿瘤治疗的共同靶点的活性改变后细胞中代谢通量的重新分布。为了实现这些目标，开发了一种化学计量代谢模型，该模型包括五个代谢途径：多胺，蛋氨酸，蛋氨酸抢救循环，叶酸循环以及谷胱甘肽和牛磺酸的合成途径。该模型基于涉及57种代谢物的51种反应，其中31种是内部代谢物。使用通量平衡分析法进行所有计算。结果表明，SAMdc的失活导致通过蛋氨酸，牛磺酸和谷胱甘肽的合成以及叶酸循环的通量显着增加。因此，当使用使SAMdc失活的治疗剂时，有必要考虑细胞肿瘤代谢重编程的可能性。S-腺苷甲硫氨酸影响丝氨酸甲基化并激活丝氨酸依赖性的从头ATP合成。蛋氨酸耗尽的细胞变得依赖于蛋氨酸，寻找新的蛋氨酸来源。SAMdc的失活增强了S-腺苷甲硫氨酸向高半胱氨酸然后向甲硫氨酸的转化。它还增强了转硫过程，激活了谷胱甘肽和牛磺酸的合成。寻找新的蛋氨酸来源。SAMdc的失活增强了S-腺苷甲硫氨酸向高半胱氨酸然后向甲硫氨酸的转化。它还增强了转硫过程，激活了谷胱甘肽和牛磺酸的合成。寻找新的蛋氨酸来源。SAMdc的失活增强了S-腺苷甲硫氨酸向高半胱氨酸然后向甲硫氨酸的转化。它还增强了转硫过程，激活了谷胱甘肽和牛磺酸的合成。