Zirconium-based metal–organic frameworks (Zr-MOFs) have shown remarkable efficacy in catalytically degrading neurotoxic agents in recent years. However, the catalytic activity of Zr-MOFs can be inhibited due to the binding of phosphate degradation products to the Zr nodes. Here, we reported the inhibition effect of a nonphosphate substance, fluoride, which can deactivate Zr-MOF nodes for the degradation of GD and VX and simulate DEPPT. The experimental and theoretical calculation results reveal that the fluoride product during GD degradation shows much more significant suppression than phosphate. The phosphate products can depart from the Zr nodes completely by adding H₂O molecules on the Zr nodes to reduce the energy barrier. However, the fluoride can replace the bridged μ₃-OH groups and terminal −OH groups on Zr-oxo clusters irreversibly, changing the electric density of Zr nodes and eliminating the terminal −OH. Without the terminal −OH, the five-coordinate phosphorus intermediate cannot be formed, resulting in the inactivation of Zr–O–Zr sites. This study provides new insights into Zr-MOF catalyst deactivation mechanisms and may help to develop a new strategy to design MOFs with high anti-inhibition efficiency for the degradation of nerve agents.

中文翻译：

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氟化物产物抑制：对 Zr-MOF 降解神经毒剂的新见解


近年来，锆基金属有机框架 （Zr-MOF） 在催化降解神经毒性药物方面显示出显着的疗效。然而，由于磷酸盐降解产物与 Zr 节点的结合，Zr-MOF 的催化活性可以被抑制。在这里，我们报道了非磷酸物质氟化物的抑制作用，它可以使 Zr-MOF 节点失活以降解 GD 和 VX 并模拟 DEPPT。实验和理论计算结果表明，GD 降解过程中的氟化物产物显示出比磷酸盐更显着的抑制作用。通过在 Zr 节点上添加 H₂O 分子以减少能垒，磷酸盐产物可以完全离开 Zr 节点。然而，氟化物可以不可逆地取代 Zr-oxo 簇上的桥接μ_3-OH 基团和末端 −OH 基团，从而改变 Zr 节点的电密度并消除末端 −OH。没有末端 −OH，五配位磷中间体就无法形成，导致 Zr-O-Zr 位点失活。本研究为 Zr-MOF 催化剂失活机制提供了新的见解，并可能有助于开发一种新策略来设计具有高抗抑制效率的 MOF 来降解神经毒剂。