Jacobasch G, Gerth C, Fabricius P G
Acta Biol Med Ger. 1977;36(3-4):587-96.
The behaviour of glycolytic flux and glycolytic metabolic concentrations was studied under conditions of magnesium deficiency. The Mg-deficiency was produced in whole animals (rats) by feeding a diet almost completely free of Mg and in hemolysates of men by the addition of a chelating agent. The results show that the decrease of the free Mg-level is diminished by partial destruction of ATP and 2,3-DPG. The analysis of the control strength of the overall flux leads to the conclusion that the decrease of the glycolytic rate is caused by an inhibition of the hexokinase-phosphofructokinase-control system. The decrease of the MgATP-Complex and free Mg++-level explains the diminished phosphorylation of glucose by the hexokinase. The ATP-inhibition of the phosphofructokinase is amplified by a small increase of free ATP-concentration and a simultaneous decrease of the Fru-6P-level. The increase of the PEP-level is caused by the diminished free Mg++ and MgATP-complex and does not demonstrate a larger control strength of the pyruvate kinase.
在镁缺乏的条件下,对糖酵解通量和糖酵解代谢物浓度的行为进行了研究。通过给全动物(大鼠)喂食几乎完全不含镁的饮食以及在人溶血产物中添加螯合剂来产生镁缺乏。结果表明,ATP和2,3 - DPG的部分破坏可减轻游离镁水平的降低。对总通量控制强度的分析得出结论,糖酵解速率的降低是由己糖激酶 - 磷酸果糖激酶控制系统的抑制引起的。MgATP复合物和游离Mg++水平的降低解释了己糖激酶对葡萄糖磷酸化作用的减弱。磷酸果糖激酶的ATP抑制作用因游离ATP浓度的小幅增加和Fru - 6P水平的同时降低而增强。PEP水平的升高是由游离Mg++和MgATP复合物的减少引起的,并且未显示丙酮酸激酶具有更大的控制强度。