Although zinc dicarboxylic acids are highly effective β-nucleating agents (β-NAs), they lose their β-nucleating ability in isotactic polypropylene (iPP) upon the addition of calcium stearate (CaStr₂). In this study, we investigated the failure mechanism of these β-NAs in terms of the chemical and physical interactions of zinc adipate (ZnAA) with CaStr₂. No chemical reaction occurs between CaStr₂ and ZnAA; rather, it is the physical interactions between this β-NA and CaStr₂ that are responsible for the loss of β-nucleating ability. Based on the experimental findings and molecular dynamics (MD) simulations, we suggest a blocking effect of CaStr₂ on nucleation as a possible failure mechanism. MD simulations confirmed that the aggregation of CaStr₂ on the β-NA surface, observed experimentally using polarized optical microscopy and scanning electron microscopy, resulted from the binding energy for the interaction between ZnAA and CaStr₂ being higher than that for iPP/CaStr₂. Because the active nucleation sites on the surface of the β-NA were covered, lattice matching between ZnAA and the iPP chains was hindered. Therefore, the addition of CaStr₂ weakens the β-nucleating ability of ZnAA, leading to inhibition of the epitaxial crystallization process, thereby decreasing the degree of β-crystal formation and, consequently, lowering the toughness of the resulting iPP.

尽管二羧酸锌是高效的β成核剂（β-NAs），但在添加硬脂酸钙（CaStr ₂）后，它们在全同立构聚丙烯（iPP）中失去了其β成核能力。在这项研究中，我们从己二酸锌（ZnAA）与CaStr ₂的化学和物理相互作用方面研究了这些β-NA的破坏机理。CaStr ₂和ZnAA之间不会发生化学反应；相反，正是这种β-NA与CaStr ₂之间的物理相互作用导致了β成核能力的丧失。根据实验结果和分子动力学（MD）模拟，我们建议CaStr ₂的阻断作用成核是一种可能的失效机制。MD模拟证实，使用偏振光学显微镜和扫描电子显微镜通过实验观察到的CaStr ₂在β-NA表面上的聚集，是由于ZnAA和CaStr ₂之间的相互作用的结合能高于iPP / CaStr ₂。因为覆盖了β-NA表面的活性成核位点，所以阻碍了ZnAA和iPP链之间的晶格匹配。因此，CaStr _2的添加减弱了ZnAA的β成核能力，导致抑制了外延结晶过程，从而降低了β晶体形成的程度，因此降低了所得iPP的韧性。