Electrochemical Generation of Single Emulsion Droplets and In Situ Observation of Collisions on an Ultramicroelectrode

The Br^–/Br₂ redox couple in aqueous solution has been often employed for redox flow batteries along with <i>N</i>-methyl-<i>N</i>-ethyl pyrrolidinium bromide (MEPBr) as a bromine-complexing agent, which forms insoluble organic droplets of MEPBr₃ complexes during electro-oxidation of Br^–. We, for the first time, report the electrochemistry of Br^– electro-oxidation in electrochemically generated single droplets of MEPBr₃ using the current transient method on an ultramicroelectrode (UME). Current spikes were observed in the chronoamperogram of the aqueous solutions containing more than 32 mM of MEPBr, and they correspond to electro-oxidation of Br^– in MEPBr₃. The voltammetric behavior of Br^– electro-oxidation in single droplets of MEPBr₃ was similar to that in the aqueous phase. The maximum concentration of Br^– in the MEPBr₃ droplets was estimated to be ∼7.5 M by fitting the observed current transient curves to the simulation using a bulk electrolysis model. Our study reveals that MEPBr₃ also plays a vital role as an electrochemical reaction medium for Br^– electro-oxidation in the Br^–/Br₂ redox system

Tuning Structures and Properties for Developing Novel Chemical Tools toward Distinct Pathogenic Elements in Alzheimer’s Disease

Multiple pathogenic factors [e.g., amyloid-β (Aβ), metal ions, metal-bound Aβ (metal–Aβ), reactive oxygen species (ROS)] are found in the brain of patients with Alzheimer’s disease (AD). In order to elucidate the roles of pathological elements in AD, chemical tools able to regulate their activities would be valuable. Due to the complicated link among multiple pathological factors, however, it has been challenging to invent such chemical tools. Herein, we report novel small molecules as chemical tools toward modulation of single or multiple target(s), designed via a rational structure-property-directed strategy. The chemical properties (e.g., oxidation potentials) of our molecules and their coverage of reactivities toward the pathological targets were successfully differentiated through a minor structural variation [i.e., replacement of one nitrogen (N) or sulfur (S) donor atom in the framework]. Among our compounds (<b>1</b>–<b>3</b>), <b>1</b> with the lowest oxidation potential is able to noticeably modify the aggregation of both metal-free Aβ and metal–Aβ, as well as scavenge free radicals. Compound <b>2</b> with the moderate oxidation potential significantly alters the aggregation of Cu­(II)–Aβ₄₂. The hardly oxidizable compound, <b>3</b>, relative to <b>1</b> and <b>2</b>, indicates no noticeable interactions with all pathogenic factors, including metal-free Aβ, metal–Aβ, and free radicals. Overall, our studies demonstrate that the design of small molecules as chemical tools able to control distinct pathological components could be achieved via fine-tuning of structures and properties