Simultaneous removal of nitrate nitrogen and orthophosphate by electroreduction and electrochemical precipitation.

Electrochemical methods can effectively remove nitrate nitrogen (NO3-N) and orthophosphate phosphorus (PO4-P) from wastewater. This work proposed a process for the simultaneous removal of NO3-N and PO4-P by combining electroreduction with electrochemically-induced calcium phosphate precipitation, and its performance and mechanisms were studied. For the treatment of 100 mg L-1 NO3-N and 5 mg L-1 PO4-P, NO3-N removal of 60-90% (per cathode area: 0.25-0.38 mg h-1 cm-2) and 80-90% (per cathode area: 0.33-0.38 mg h-1 cm-2) could be acquired within 3 h in single-chamber cell (SCC) and dual-chamber cell (DCC), while P removal was 80-98% (per cathode area: 0.10-0.12 mg h-1 cm-2) in SCC after 30 min and 98% (per cathode area: 0.37 mg h-1 cm-2) in DCC within 10 min. The faster P removal in DCC was due to the higher pH and more abundant Ca2+ in the cathode chamber of DCC, which was caused by the cation exchange membrane (CEM). Interestingly, NO3-N reduction enhanced P removal because more OH- can be produced by nitrate reduction than hydrogen evolution for an equal-charge reaction. For 10 mg L-1 PO4-P in SCC, when the initial NO3-N was 0, 20, 100, and 500 mg L-1, the P removal efficiencies after 1 h treatment were < 10%, 45-55%, 86-99%, and above 98% respectively. An increase in Ca2+ concentration also promoted P removal. However, Ca and P inhibited nitrate reduction in SCC at the relatively low initial Ca/P, as CaP on the cathode limited the charge or mass transfer process. The removal efficiency of NO3-N in SCC after 3 h reaction can reduce by about 17%, 40%, and 34% for Co3O4/Ti, Co/Ti, and TiO2/Ti. The degree of inhibition of P on NO3-N removal was related to the content and composition of CaP deposited on the cathode. On the cathode, the lower the deposited Ca and P, and the higher the deposited Ca/P molar ratio, the weaker the inhibition of P on NO3-N removal. Especially, P had little or even no inhibition on nitrate reduction when treated in DCC instead of SCC or under high initial Ca/P. It is speculated that under these conditions, a high local pH and local high concentration Ca2+ layer near the cathode led to a decrease in CaP deposition and an increase in Ca/P molar ratio on the cathode. High initial concentrations of NO3-N might also be beneficial in reducing the inhibition of P on nitrate reduction, as few CaP with high Ca/P molar ratios were deposited on the cathode. The evaluation of the real wastewater treatment was also conducted.

Emodin attenuates cardiomyocyte pyroptosis in doxorubicin-induced cardiotoxicity by directly binding to GSDMD.

BACKGROUND: Doxorubicin (Dox), which is an anticancer drug, has significant cardiac toxicity and side effects. Pyroptosis occurs during Dox-induced cardiotoxicity (DIC), and drug inhibition of this process is one therapeutic approach for treating DIC. Previous studies have indicated that emodin can reduce pyroptosis. However, the role of emodin in DIC and its molecular targets remain unknown. HYPOTHESIS/PURPOSE: We aimed to clarify the protective role of emodin in mitigating DIC, as well as the mechanisms underlying this effect. METHODS: The model of DIC was established via the intraperitoneal administration of Dox at a dosage of 5 mg/kg per week for a span of 4 weeks. Emodin at two different doses (10 and 20 mg/kg) or a vehicle was intragastrically administered to the mice once per day throughout the Dox treatment period. Cardiac function, myocardial injury markers, pathological morphology of the heart, level of pyroptosis and mitochondrial function were assessed. Protein microarray, biolayer interferometry and pull-down assays were used to confirm the target of emodin. Moreover, GSDMD-overexpressing plasmids were transfected into GSDMD-/- mice and HL-1 cells to further verify whether emodin suppressed GSDMD activation. RESULTS: Emodin therapy markedly enhanced cardiac function and reduced cardiomyocyte pyroptosis in mice induced by Dox. Mechanistically, emodin binds to GSDMD and inhibits the activation of GSDMD by targeting the Trp415 and Leu290 residues. Moreover, emodin was able to mitigate Dox-induced cardiac dysfunction and myocardial injury in GSDMD-/- mice overexpressing GSDMD, as shown by increased EF and FS, decreased serum levels of CK-MB, LDH and IL-1ß and mitigated cell death and cell morphological disorder. Additionally, emodin treatment significantly reduced GSDMD-N expression and plasma membrane disruption in HL-1 cells overexpressing GSDMD induced by Dox. In addition, emodin reduced mitochondrial damage by alleviating Dox-induced GSDMD perforation in the mitochondrial membrane. CONCLUSION: Emodin has the potential to attenuate DIC by directly binding to GSDMD to inhibit pyroptosis. Emodin may become a promising drug for prevention and treatment of DIC.