Electron transfer-mediated enhancement of superoxide radical generation in fenton-like process: Key role of oxygen vacancy-regulated local electron density of cobalt sites

Designing metal oxides with oxygen vacancy (OV) is a prospective strategy for boosted Fenton-like process. However, what OV is, whether OV enhancement increases the catalytic performance, OV-related H2O2 activation, and relationship between OV and ROS or non-radical pathways have not been fully understood. Herein, yolk-shell Co3O4 nanospheres with various OV were fabricated to overcome the above contentious problems and establish a relationship between OV, ROS, and electron transfer in sulfadiazine (SDZ) degradation via H2O2 activation. The results showed that the delocalized electron-rich Co sites around OV with increasing OV allowed the improved conductivity, thereby leading to stronger adsorption and activation of H2O2 to generate more (OH)-O-center dot as evidenced by the attenuated adsorption energy and prolonged O-O bond. The subsequent rapid depletion of (OH)-O-center dot coupled with the increase in O-2(center dot-) over time and the emergence of electron transfer from SDZ explored a pathway enhancing O-2(center dot-) generation for SDZ degradation.

Automated summary

Designing metal oxides with oxygen vacancies (OVs) is a potential strategy for improving the Fenton-like process. However, the nature of OV, the effect of OV enhancement on catalytic performance, the activation of H2O2 by OV, and the relationship between OV and ROS or non-radical pathways are not fully understood. In this study, yolk-shell Co3O4 nanospheres with varying OV were synthesized to investigate the relationship between OV, ROS, and electron transfer in the degradation of sulfadiazine (SDZ) via H2O2 activation. The results showed that the increased OV led to improved conductivity and enhanced adsorption and activation of H2O2, resulting in the generation of more hydroxyl radicals and promoting the degradation of SDZ through increased production of superoxide radicals.