HMOX2

The heterogeneous loss of HO₂ radicals onto ambient aerosols plays an important role in tropospheric chemistry. However, sparse investigation of the dominating parameters controlling the HO₂ uptake coefficients onto ambient aerosols (γHO₂) has largely hindered the application of the measured γHO₂ to the global spatial prediction. Here we induced an offline method using LFP-LIF technique to measure the kinetics of HO₂ uptake onto ambient aerosols collected in summertime and wintertime in Yokohama city, a regional urban site near Tokyo, Japan. By controlling the dominating parameters which influence γHO₂, we were able to investigate the detailed HO₂ uptake mechanism. We characterized the chemical composition of the collected ambient aerosols, including organics, inorganics, transition metals ions, etc. and modeled γHO₂ using different mechanisms. Results show that γHO₂ increased with the increase in RH, and the aerosol states ("dry" or wet/aqueous) have large effects on γHO₂. With fixed RH and aerosol chemical composition, γHO₂was highly dependent on pH and inversely correlated with [HO₂]₀. By combing the measured γHO₂ values with the modeled ones, we found that both the HO₂ self-reaction and transition metal-catalyzed reactions should be accounted for to yield a single parameterization to predict γHO₂, and different chemical compositions may have collective effects on γHO₂. Results may serve for extending the γHO₂ values measured at one observation site to different environmental conditions, which will help us to achieve more accurate modeling results concerning secondary pollutant formation (i.e., ozone).

Dechlorination of chloropyridines can eliminate their detrimental environmental effects. However, traditional dechlorination technology cannot efficiently break the C-Cl bond of chloropyridines, which is restricted by the uncontrollable nonselective species. Hence, we propose the carbonate species-activated hydrogen peroxide (carbonate species/H₂O₂) process wherein the selective oxidant (peroxymonocarbonate ion, HCO₄^-) and selective reductant (hydroperoxide anion, HO₂^-) controllably coexist by manipulation of reaction pH. Taking 2-chloropyridine (Cl-Py) as an example, HCO₄^- first induces Cl-Py into pyridine N-oxidation intermediates, which then suffer from the nucleophilic dechlorination by HO₂^-. The obtained dechlorination efficiencies in the carbonate species/H₂O₂ process (32.5-84.5%) based on the cooperation of HCO₄^- and HO₂^- are significantly higher than those in the HO₂^--mediated sodium hydroxide/hydrogen peroxide process (0-43.8%). Theoretical calculations confirm that pyridine N-oxidation of Cl-Py can effectively lower the energy barrier of the dechlorination process. Moreover, the carbonate species/H₂O₂ process exhibits superior anti-interference performance and low electric energy consumption. Furthermore, Cl-Py is completely detoxified via the carbonate species/H₂O₂ process. More importantly, the carbonate species/H₂O₂ process is applicable for efficient dehalogenation of halogenated pyridines and pyrazines. This work offers a simple and useful strategy to enhance the dehalogenation efficiency of halogenated organics and sheds new insights into the application of the carbonate species/H₂O₂ process in practical environmental remediation.

Ten-eleven translocation enzymes (TETs) are Fe(II)/2-oxoglutarate (2OG) oxygenases that catalyze the sequential oxidation of 5-methylcytosine to 5-hydroxymethylcytosine, 5-formylcytosine, and 5-carboxylcytosine in eukaryotic DNA. Despite their roles in epigenetic regulation, there is a lack of reported TET inhibitors. The extent to which 2OG oxygenase inhibitors, including clinically used inhibitors and oncometabolites, modulate DNA modifications via TETs has been unclear. Here, we report studies on human TET1-3 inhibition by a set of 2OG oxygenase-focused inhibitors, employing both enzyme-based and cellular assays. Most inhibitors manifested similar potencies for TET1-3 and caused increases in cellular ^5hmC levels. (R)-2-Hydroxyglutarate, an oncometabolite elevated in isocitrate dehydrogenase mutant cancer cells, showed different degrees of inhibition, with TET1 being less potently inhibited than TET3 and TET2, potentially reflecting the proposed role of TET2 mutations in tumorigenesis. The results highlight the tractability of TETs as drug targets and provide starting points for selective inhibitor design.