Defective multi-element hydroxides nanosheets for rapid removal of anionic organic dyes from water and oxygen evolution reaction.

Water pollution by dyes is one of the biggest environmental problems. Adsorption technology has been widely used in wastewater treatment. In this work, high-entropy concept is used to design surface defective hydroxides realizing the rapid removal of dyes from water. Multi-element hydroxides (MEHs) containing three (CoMnNi, MEH-Ternary), four (CoMnNiZn, MEH-Quaternary), and five (CoMnNiZnFe, MEH-Quinary) metal elements are successfully synthesized through a polyol process. These as-synthesized MEHs are composed of nanosheets with a brucite-like structure. Along with the increase in compositional complexity (i.e., configurational entropy), the thickness of the nanosheets in these MEHs decreases, while the degree of surface defects increase. These surface defects are probably the active sites for anionic dyes adsorption, suggesting rapid adsorption kinetics with shortened diffusion path length. For MEH-Quinary in 0.2 mM Congo red (CR) and MEH-Ternary in 0.4 mM methyl orange (MO) aqueous solutions, respectively, high removal efficiency > 99.0% is achieved in the first 30 s. Their pseudo-second-order rate constants are two orders of magnitude higher than that of activated carbon and hydrotalcite. MEH-Quinary has maximum CR and MO adsorption quantity of 546.4 and 404.9 mg g-1, respectively, by Langmuir model. The MEH-Quinary is also a potential electrocatalyst for oxygen evolution reaction.

2,2,6,6-Tetramethylpiperidine-1-oxyl acts as a volatile inhibitor of ferroptosis and neurological injury.

Ferroptosis, a type of oxidative stress cell death, has been implicated in cell injury in several diseases, and treatments with specific inhibitors have been shown to protect cells and tissues. Here we demonstrated that a treatment with the nitroxide radical, 2,2,6,6-tetramethylpiperidine-N-oxyl (TEMPO), prevented the ferroptotic cell death in an airborne manner. Other TEMPO derivatives and lipophilic antioxidants, such as Trolox and ferrostatin-1, also prevented cell death induced by erastin and RSL3; however, only TEMPO exhibited inhibitory activity from a physically distant location. TEMPO vaporized without decomposing and then dissolved again into a nearby water solution. Volatilized TEMPO inhibited glutamate-induced cell death in mouse hippocampal cell lines and also reduced neuronal cell death in a mouse ischemia model. These results suggest that TEMPO is a unique cell protective agent that acts in a volatility-mediated manner.