New insights into clopyralid degradation by sulfate radical: Pyridine ring cleavage pathways.

Contamination by herbicides such as clopyralid (CLP) poses a significant threat to human health and ecological systems. In the present study, efficient removal of CLP was achieved by thermo activated persulfate, among which sulfate radical was identified as the predominant oxidizing species responsible for the decontamination. Based on high resolution LC-MS, derivatization method and density functional theory (DFT) computation, the detailed oxidation pathways and mechanisms were proposed. The primary oxidation pathways included dechlorination-hydroxylation, decarboxylation and the formation of quinone-like moieties. Afterwards, numerous intermediate byproducts ranging from high molecular to very small ones were identified, suggesting the pyridine ring was damaged during the thermo activated persulfate process. The detected products containing six and five carbons indicated the pyridine ring cleavage would take place on the quinone-structure intermediate. Further oxidation could continue by breaking each bond on the ring-cleavage product, yielding a series of short-chain carbonyl chemicals, carboxylic acids and inorganic ions. In addition, the presence of dissolved oxygen (DO) was favorable to CLP degradation, indicating DO played an important role in applying such technology. The degradation rate constants of CLP increased appreciably with increasing temperature, and acidic pH facilitated the CLP degradation. The results obtained in this work would increase our understanding on the environmental fates of nitrogen heterocyclic compounds during sulfate radical (SO4•-)-based advanced oxidation processes (SR-AOPs).

Triggering the succinate receptor GPR91 enhances pressure overload-induced right ventricular hypertrophy.

BACKGROUND: Pulmonary arterial hypertension (PAH) leads to pressure overload in the right ventricle (RV) and induces right ventricular hypertrophy (RVH). GPR91 is an orphan G-protein-coupled receptor (GPCR) that has been characterized as a receptor for succinate, which increases in RVH; however, its role remains unknown. METHODS AND RESULTS: We studied succinate-GPR91 signaling in a pulmonary arterial banding (PAB) model of RVH in the SD rats due to pressure overload. We report that GPR91 was located in cardiomyocytes. We found that the expressions of GPR91 and p-Akt in the RV significantly increased in the PAB model compared with the sham. In the PAB rats, the treatment of succinate further increased the p-Akt levels and aggravated RVH in vivo. In in vitro studies, succinate stimulated the up-regulation of the hypertrophic gene marker anp. All these effects were inhibited by the antagonist of PI3K, wortmannin, both in vivo and in vitro. Finally, we found that the GPR91-PI3K/Akt axis was also up-regulated compared with the sham in human RVH. CONCLUSIONS: Our results suggest that succinate-GPR91 is involved in RVH via PI3K/Akt signaling in vivo and in vitro. GPR91 may be a novel therapeutic target for RVH induced by pressure overload.