Strategies for promoting the degradation of phenol by electro-Fenton: Simultaneously promoting the generation and utilization of H2O2.

The use of the electro-Fenton process to continuously generate H2O2 and efficiently degrade organic pollutants is considered a promising technology. The ratio of generation of H2O2 is usually regarded as the critical step; however, how the H2O2 is utilized is also of particular importance. Herein, activated carbon was activated at different temperatures and used to explore the effect of nitrogen doping on the production and utilization of H2O2 in the electro-Fenton-based degradation of organic pollutants. The experimental results indicate that nitrogen-doped activated carbon simultaneously promotes the generation and utilization of H2O2, which is attributed to the regulation of the competition between phenol and O2 adsorption by the doped nitrogen. Nitrogen doping not only improves 2e-ORR selectivity but also aggregates phenol near the cathode to balance the concentrations of phenol and ·OH. Density functional theory (DFT) calculations further confirmed that pyrrole-N as a dopant promoted the adsorption of phenol, while pyridine-N was more favorable for O2 adsorption. The unique balance of nitrogen types possessed by modified activated carbon NAC-750 permits the efficient synergistic generation and utilization of H2O2 in a balanced manner during the degradation of phenol. This work provides a new direction for the rational nitrogen-doping modification of activated carbon for the electro-Fenton-based degradation of organic pollutants.

Carbon Monoxide-Saturated Hemoglobin-Based Oxygen Carriers Attenuate High-Altitude-Induced Cardiac Injury by Amelioration of the Inflammation Response and Mitochondrial Oxidative Damage.

OBJECTIVE: To investigate the therapeutic effect of carbon monoxide (CO) on high-altitude hypoxia-induced cardiac damage. METHODS: Forty male C57BL/6 mice were randomly divided into 4 groups. The mice were exposed to normoxia or simulated 5,500-meter high-altitude hypoxia in a hypobaric chamber for 7 days. During the first 3 days, the mice were pretreated with CO-saturated hemoglobin (Hb)-based oxygen carrier (CO-HBOC), oxygen-saturated hemoglobin-based oxygen carrier (O2-HBOC) at a dose of 0.3 g Hb/kg/day or an equivalent volume of saline. The in vivo left ventricle function, cardiac enzyme release, histopathological changes, apoptosis and inflammation were also measured. RESULTS: High-altitude hypoxia induced significant cardiac damage, as demonstrated by impaired cardiac function and increased proapoptotic, proinflammatory and pro-oxidant markers. Pretreatment with CO-HBOC significantly improved cardiac performance, reduced cardiac enzyme release and limited myocardial apoptosis. The increased inflammatory response was also suppressed. In addition to the preserved mitochondrial structure, hypobaric hypoxia-induced mitochondrial oxidative damage was remarkably attenuated. Moreover, these antiapoptotic and antioxidative effects were accompanied by an upregulated phosphorylation of Akt, ERK and STAT3. CONCLUSION: This study demonstrated that CO-HBOC provides a promising protective effect on high-altitude hypoxia-induced myocardial injury, which is mediated by the inhibition of inflammation and mitochondrial oxidative damage.