Search

On the catalyst surface, crystal facets with different surface atom arrangements and diverse physicochemical properties lead to distinct catalytic activity. Acquiring a highly reactive facet through surface regulation is an efficient strategy to promote the oxidative decomposition of wastewater organic pollutants via peroxymonosulfate (PMS) activation. However, the mechanism through which crystal facets affect PMS activation is still unclear. In this study, three facet-engineered α-MnO2 with different exposed facets were prepared via a facile hydrothermal route. The prepared 310-MnO2 exhibited superior PMS activation performance to 100-MnO2 and 110-MnO2. Moreover, the 310-MnO2/PMS oxidative system was active over a wide pH range and highly resistant to interfering substances from wastewater. These advantages of the 310-MnO2/PMS system make it highly promising for practical wastewater treatment. Based on quenching experiments, electron paramagnetic resonance (EPR) analysis, solvent exchange, and electrochemical measurements, mediated electron transfer was found to be the dominant nonradical pathway for p-chloroaniline (PCA) degradation. A sulfhydryl group (-SH) masking experiment showed that the highly exposed Mn atoms on the 310-MnO2 surface were sites of PMS activation. In addition, density functional theory (DFT) calculations confirmed that the dominant {310} facet promoted adsorption/activation of PMS, which favored the formation of more metastable complexes on the α-MnO2 surface. The reaction mechanism obtained here clarifies the relationship between PMS activation and crystal facets. This study provides significant insights into the rational design of high-performance catalysts for efficient water remediation.

Abnormal energy metabolism is a characteristic of tumor cells, and mitochondria are important components of tumor metabolic reprogramming. Mitochondria have gradually received the attention of scientists due to their important functions, such as providing chemical energy, producing substrates for tumor anabolism, controlling REDOX and calcium homeostasis, participating in the regulation of transcription, and controlling cell death. Based on the concept of reprogramming mitochondrial metabolism, a range of drugs have been developed to target the mitochondria. In this review, we discuss the current progress in mitochondrial metabolic reprogramming and summarized the corresponding treatment options. Finally, we propose mitochondrial inner membrane transporters as new and feasible therapeutic targets.