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Abstract α‐substituted ketones are important chemical targets as synthetic intermediates as well as functionalities in natural products and pharmaceuticals. We report the α‐acetylation of C(sp³)−H substrates R−H with arylmethyl ketones ArC(O)Me to provide α‐alkylated ketones ArC(O)CH₂R at RT with^tBuOO^tBu as oxidant via copper(I) ‐diketiminato catalysts. Proceeding via alkyl radicals R•, this method enables α‐substitution with bulky substituents without competing elimination that occurs in more traditional alkylation reactions between enolates and alkyl electrophiles. DFT studies suggest the intermediacy of copper(II) enolates [Cu^II](CH₂C(O)Ar) that capture alkyl radicals R• to give R−CH₂C(O)Ar outcompeting dimerization of the copper(II) enolate to give the 1,4‐diketone ArC(O)CH₂CH₂C(O)Ar. 

Reversible cyclopropane formation is examined in a chromium diamide–diimine chelate complexviareduction. Sites of electrophilicity incur similar and divergent chemistry; structural, electrochemical, and calculational studies afford their rationale. 

The electrochemical reduction of nitrate to ammonia is of interest as an energy/environmentally friendly source of ammonia for agriculture and energy applications and as a route toward groundwater purification. We report in situ photoemission data, electrochemical results, and density functional theory calculations that demonstrate vanadium oxide—prepared by ambient exposure of V metal, with a distribution of surface V³⁺and V⁴⁺oxidation states—specifically adsorbs and reduces nitrate to ammonia at pH 3.2 at cathodic potentials. Negligible cathodic activity in the absence of NO₃⁻indicates high selectivity with respect to non-nitrate reduction processes. In situ photoemission data indicate that nitrate adsorption and reduction to adsorbed NO₂is a key step in the reduction process. NO₃RR activity is also observed at pH 7, albeit at a much slower rate. The results indicate that intermediate (non-d⁰) oxidation states are important for both molecular nitrogen and nitrate reduction to ammonia. 

Abstract DNA methylation at cytosine bases (5-methylcytosine, 5mC) is a heritable epigenetic mark regulating gene expression. While enzymes that metabolize 5mC are well-characterized, endogenous signaling molecules that regulate DNA methylation machinery have not been described. We report that physiological nitric oxide (NO) concentrations reversibly inhibit the DNA demethylases TET and ALKBH2 by binding to the mononuclear non-heme iron atom forming a dinitrosyliron complex (DNIC) and preventing cosubstrates from binding. In cancer cells treated with exogenous NO, or endogenously synthesizing NO, 5mC and 5-hydroxymethylcytosine (5hmC) increase, with no changes in DNA methyltransferase activity. 5mC is also significantly increased in NO-producing patient-derived xenograft tumors from mice. Genome-wide methylome analysis of cells chronically treated with NO (10 days) shows enrichment of 5mC and 5hmC at gene-regulatory loci, correlating with altered expression of NO-regulated tumor-associated genes. Regulation of DNA methylation is distinctly different from canonical NO signaling and represents a unique epigenetic role for NO.