Mechanism of Pd(OAc)2/pyridine catalyst reoxidation by O2: influence of labile monodentate ligands and identification of a biomimetic mechanism for O2 activation.

The mechanism of catalyst oxidation by O(2) in Pd-catalyzed aerobic oxidation reactions has been the subject of considerable debate, particularly with respect to the reactivity of Pd(II)-hydride species. Here, we describe the use of unrestricted DFT computational methods to investigate the mechanism of catalyst reoxidation with the Pd(OAc)(2)/pyridine catalyst system, one of the most widely used catalysts. These studies probe four different pathways for the formation of a Pd(II)-hydroperoxide species from the reaction of O(2) from the corresponding Pd(II)-hydride [(py)(n)Pd(II)(H)OAc]: 1) a homolytic pathway involving hydrogen-atom abstraction by O(2); 2) AcOH reductive elimination to yield a Pd(0) species that subsequently reacts with O(2); 3) migratory insertion of O(2) into a Pd-H bond; and 4) oxidative addition of O(2) to Pd(II) to yield a Pd(IV)(eta(2)-peroxo) species. In contrast to previous studies of reactions between O(2) and Pd-hydride species, the reductive-elimination pathway (mechanism 2) is significantly more favorable than any of the other pathways. This outcome is traced to the presence of labile ligands (pyridine) that can readily dissociate from Pd to enable the hydride and acetate ligands to occupy cis-coordination sites. These results strongly support the involvement of Pd(0) as an intermediate in the catalytic cycle. Investigations of the mechanism of the reaction of O(2) with the Pd(0) intermediate revealed a novel, previously unrecognized mechanism that yields a Pd-OOH product without proceeding through the intermediacy of a Pd(II)(eta(2)-peroxo) species. This mechanism resembles pathways commonly observed in biological O(2) activation and suggests that noble-metal and biological oxidation mechanisms may be more similar than previously appreciated.