Wolf F I, Bossi D, Cittadini A
Institute of General Pathology, Catholic University, School of Medicine, Italy.
Biochem Biophys Res Commun. 1991 Sep 16;179(2):1000-5. doi: 10.1016/0006-291x(91)91917-2.
We have previously observed that extracellular Mg2+ influences the phosphofructokinase (PFK) activity of intact Ehrlich Ascites tumour cells (EATC). In this study we have investigated the mechanism by which Mg2+ modulates this key glycolytic enzyme in EATC made permeable to the cation by either digitonin or dextran sulphate. Results showed that when Mg2+ is freely permeable to the cytosol, the in vivo PFK activity, calculated as FDP/G6P ratio, is not increased as it is in intact cells. We also observed that in permeabilized cells Mg2+ determines the increase of glucose 6 phosphate (G6P), fructose 1,6 bisphosphate (FDP) and lactate production. We hypothesize that extracellular Mg2+ regulates PFK and glycolysis in these neoplastic cells not by entering the cytosol but by a specific interaction with the plasma membrane.
我们之前观察到细胞外镁离子(Mg2+)会影响完整的艾氏腹水瘤细胞(EATC)中磷酸果糖激酶(PFK)的活性。在本研究中,我们调查了Mg2+调节这种关键糖酵解酶的机制,该机制发生在通过洋地黄皂苷或硫酸葡聚糖使阳离子具有通透性的EATC中。结果显示,当Mg2+可自由通透进入细胞质时,以FDP/G6P比值计算的体内PFK活性并不像在完整细胞中那样增加。我们还观察到,在通透化细胞中,Mg2+会导致葡萄糖6磷酸(G6P)、果糖1,6二磷酸(FDP)和乳酸产量增加。我们推测,细胞外Mg2+并非通过进入细胞质,而是通过与质膜的特异性相互作用来调节这些肿瘤细胞中的PFK和糖酵解。