Ackermann B P, Ahlers J
Biochem J. 1976 Feb 1;153(2):151-7. doi: 10.1042/bj1530151.
Metal ion-complexing agents, like KCN, EDTA etc., inactivate alkaline phosphatase of pig kidney. This inactivation is reversible at low concentrations of the complexing agents and irreversible at high concentrations. The reversible inhibition is probably due to removal of Zn2+ ions from the active site, where they are necessary for catalytic action, whereas the irreversible inhibition results from the removal of Zn2+ ions necessary for preservation of the structure. The inactivation is pseudo-first order. It depends on the concentration, size and charge of the complexing agents. Beta-Glycerophosphate and Mg2+ ions protect the enzyme from inactivation by complexing agents. Quantitative examination of the effect of substrate leads to a model that is similar to the "sequential model" proposed by D.E. Koshland, G. Nemethy & D. Filmer (1966) (Biochemistry 5, 365-385) to explain allosteric behavior of enzymes. It describes the sequential addition of two substrate molecules at two active centres of the dimer enzyme. The binding of the substrate molecules is accompanied by changes in the conformation, which lead to stabilization of the enzyme against attack by complexing agents.
金属离子络合剂,如氰化钾、乙二胺四乙酸等,会使猪肾碱性磷酸酶失活。在低浓度络合剂时,这种失活是可逆的,而在高浓度时则是不可逆的。可逆抑制可能是由于从活性位点去除了锌离子,而锌离子对于催化作用是必需的,而不可逆抑制则是由于去除了维持结构所需的锌离子。失活是准一级反应。它取决于络合剂的浓度、大小和电荷。β-甘油磷酸酯和镁离子可保护酶不被络合剂失活。对底物效应的定量研究得出了一个模型,该模型类似于D.E. 科什兰德、G. 内梅西和D. 菲尔默(1966年)(《生物化学》5卷,365 - 385页)提出的“顺序模型”,用于解释酶的别构行为。它描述了两个底物分子在二聚体酶的两个活性中心依次添加的过程。底物分子的结合伴随着构象变化,这导致酶对络合剂的攻击具有稳定性。