Practical and regioselective halonitrooxylation of olefins to access ß-halonitrates.

Organic nitrates, as effective donors of the signaling molecule nitric oxide, are widely applied in the pharmaceutical industry. However, practical and efficient methods for accessing organic nitrates are still scarce, and achieving high regiocontrol in unactivated alkene difunctionalization remains challenging. Here we present a simple and practical method for highly regioselective halonitrooxylation of unactivated alkenes. The approach utilizes TMSX (X: Cl, Br, or I) and oxybis(aryl-λ3-iodanediyl) dinitrates (OAIDN) as sources of halogen and nitrooxy groups, with 0.5 mol % FeCl3 as the catalyst. Remarkably, high regioselectivity in the halonitrooxylation of aromatic alkenes can be achieved even without any catalyst. This protocol features easy scalability and excellent functional group compatibility, providing a range of ß-halonitrates (127 examples, up to 99% yield, up to >20:1 rr). Notably, 2-iodoethyl nitrate, a potent synthon derived from ethylene, reacts smoothly with a variety of functional units to incorporate the nitrooxy group into the desired molecules.

Enantioselective copper-catalyzed azidation/click cascade reaction for access to chiral 1,2,3-triazoles.

Chiral 1,2,3-triazoles are highly attractive motifs in various fields. However, achieving catalytic asymmetric click reactions of azides and alkynes for chiral triazole synthesis remains a significant challenge, mainly due to the limited catalytic systems and substrate scope. Herein, we report an enantioselective azidation/click cascade reaction of N-propargyl-ß-ketoamides with a readily available and potent azido transfer reagent via copper catalysis, which affords a variety of chiral 1,2,3-triazoles with up to 99% yield and 95% ee under mild conditions. Notably, chiral 1,5-disubstituted triazoles that have not been accessed by previous asymmetric click reactions are also prepared with good functional group tolerance.

Unraveling the toxicity response and metabolic compensation mechanism of tannic acid-Cr(III) complex on alga Raphidocelis subcapitata.

Due to their assembly properties and variable molecular weights, the potential biological toxicity effects of macromolecular organic ligand heavy metal complexes are more difficult to predict and their mechanisms are more complex. This study unraveled the toxicity response and metabolic compensation mechanism of tannic acid-Cr(III) (TA-Cr(III)) complex on alga Raphidocelis subcapitata using multi-omics approaches. Results showed TA-Cr(III) complex caused oxidative damage and photosystem disruption, destroying the cell morphology and inhibiting algal growth by >80 % at high exposure levels. TA-Cr(III) complex stress down-regulated proteins linked to proliferation, photosynthesis and antioxidation while upregulating carbon fixation, TCA cycle and amino acid metabolism. The increase of fumarate, citrate, isocitrate and semialdehyde succinate was validated by metabolomics analysis, which improved the TCA cycle, amino acid metabolism and carbon fixation. Activation of the above cellular processes somewhat compensated for the inhibition of algal photosynthesis by TA-Cr(III) complex exposure. In conclusion, physiological toxicity coupled with downstream metabolic compensation in response to Cr(III) complex of macromolecular was characterized in Raphidocelis subcapitata, unveiling the adaptive mechanism of algae under the stress of heavy metal complexes with macromolecular organic ligands.