Sub‑3 nm CoO Nanoparticles with Oxygen Vacancy-Dependent Catalytic Activity for the Oxygen Reduction Reaction

Developing transition metal-based electrocatalysts toward the oxygen reduction reaction (ORR) with high activity has attracted much attention for high-powered electrochemical energy conversion devices. Earth-abundant and low-cost cobalt oxide has attracted ever-growing interest; however, insufficient active sites and poor electrical conductivity hamper the improvement of catalytic activity for the ORR. Herein, the high-dispersed ultra-small CoO nanoparticles on three-dimensional porous carbon are synthesized by a facile wet chemistry and low-temperature calcination strategy. The characterization with multiple techniques shows that the oxygen vacancy defects are in situ formed on sub-3 nm CoO, and oxygen vacancy concentrations can be adjusted to investigate the related ORR performance. The computational and experimental results demonstrate that moderate oxygen vacancy concentration in CoO improves electrical conductivity, reduces the energy barrier in the rate-limiting step, and optimizes the adsorption of *O and *OH intermediates, thus achieving a high half-wave potential of 0.80 V and a limiting current density of 5.26 mA cm–2. This work points out an avenue to the future design of high-efficiency metal oxides for diverse renewable energy applications

Selenomethionine Alleviates DON-Induced Oxidative Stress <i>via</i> Modulating Keap1/Nrf2 Signaling in the Small Intestinal Epithelium

The small intestinal epithelium is regulated in response to various beneficial or harmful environmental information. Deoxynivalenol (DON), a mycotoxin widely distributed in cereal-based feeds, induces oxidative stress damage in the intestine due to the mitochondrial stress. As a functional nutrient, selenomethionine (Se-Met) is involved in synthesizing several antioxidant enzymes, yet whether it can replenish the intestinal epithelium upon DON exposure remains unknown. Therefore, the in vivo model C57BL/6 mice and the in vitro model MODE-K cells were treated with l-Se-Met and DON alone or in combination to confirm the status of intestinal stem cell (ISC)-driven epithelial regeneration. The results showed that 0.1 mg/kg body weight (BW) Se-Met reinstated the growth performance and integrity of jejunal structure and barrier function in DON-challenged mice. Moreover, Lgr5+ ISCs and PCNA+ mitotic cells in crypts were prominently increased by Se-Met in the presence of DON, concomitant with a significant increase in absorptive cells, goblet cells, and Paneth cells. Simultaneously, crypt-derived jejunal organoids from the Se-Met + DON group exhibited more significant growth advantages ex vivo. Furthermore, Se-Met-stimulated Keap1/Nrf2-dependent antioxidant system (T-AOC and GSH-Px) to inhibit the accumulation of ROS and MDA in the jejunum and serum. Moreover, Se-Met failed to rescue the DON-triggered impairment of cell antioxidant function after Nrf2 perturbation using its specific inhibitor ML385 in MODE-K cells. In conclusion, Se-Met protects ISC-driven intestinal epithelial integrity against DON-induced oxidative stress damage by modulating Keap1/Nrf2 signaling