A Coupled System of Ni3S2 and Rh Complex with Biomimetic Function for Electrocatalytic 1,4-NAD(P)H Regeneration.

NAD(P)H cofactor is a critical energy and electron carrier in biocatalysis and photosynthesis, but the artificial reduction of NAD(P)+ to regenerate bioactive 1,4-NAD(P)H with both high activity and selectivity is challenging. Herein, we found that a coupled system of a Ni3S2 electrode and a Rh complex in an electrolyte (denoted as Ni3S2-Rh) can catalyze the reduction of NAD(P)+ to 1,4-NAD(P)H with superior activity and selectivity. The optimized selectivity in 1,4-NADH can be up to 99.1%, much higher than that for Ni3S2 (80%); the normalized activity of Ni3S2-Rh is about 5.8 times that of Ni3S2 and 13.2 times that of the Rh complex. The high performance of Ni3S2-Rh is attributed to the synergistic effect between metal sulfides and Rh complex. The NAD+ reduction reaction proceeds via a concerted electron-proton transfer (CEPT) mechanism in the Ni3S2-Rh system, in which Ni3S2 acts as a proton and electron-transfer mediator to accelerate the formation of Rh hydride (Rh-H), and then the Rh-H regioselectively transfers the hydride to NAD+ to form 1,4-NADH. The artificial system Ni3S2-Rh essentially mimics the functions of ferredoxin-NADP+ reductase in nature.

A responsive anionic wormlike micelle using pH-directed release of stored sodium based on polybasic acids.

Responsive wormlike micelles are very useful in a number of applications, whereas it is still challenging to create dramatic viscosity changes in anionic surfactant systems. Here a differential pH-responsive wormlike micelle based on sulfonic surfactants was developed, which is formed by mixing sodium dodecyl trioxyethylene sulphate (SDES) and ethylenediaminetetraacetic acid tetrasodium (EDTA4-·4Na+) at the molar ratio of 1 : 1. The phase behavior, aggregate microstructure and viscoelasticity of the SDES/EDTA4-·4Na+ solution were investigated via macroscopic observation, cryo-TEM and rheological measurements. It was found that the phase behavior of the SDES/EDTA4-·4Na+ solution undergoes transitions from a water-like fluid to viscoelastic upon decreasing the pH. On decreasing the pH from 12.01 to 3.27 by adding HCl, the viscosity of the transparent solutions with wormlike micelles was increased rapidly and reached ∼3100 mPa s. Furthermore, on increasing the pH by adding NaOH, the viscosity was slightly increased due to the addition of Na+. However, the increase in the concentration of Na+ is much smaller than the theoretical addition. The same phenomenon was noted in the sodium citrate solution, but does not exist in the sodium formate system. The viscosity of the micellar solution has a sensitive response to inorganic acids and tolerance to inorganic bases due to the characteristics of polybasic acids.

Emerging nanomaterials targeting macrophage adapted to abnormal metabolism in cancer and atherosclerosis therapy (Review).

Macrophages, as highly heterogeneous and plastic immune cells, occupy a pivotal role in both pro­inflammatory (M1) and anti­inflammatory (M2) responses. While M1­type macrophages secrete pro­inflammatory factors to initiate and sustain inflammation, M2­type macrophages promote inflammation regression and uphold tissue homeostasis. These distinct phenotypic transitions in macrophages are closely linked to significant alterations in cellular metabolism, encompassing key response pathways such as glycolysis, pentose phosphate pathway, oxidative phosphorylation, lipid metabolism, amino acid metabolism, the tricarboxylic acid cycle and iron metabolism. These metabolic adaptations enable macrophages to adapt their activities in response to varying disease microenvironments. Therefore, the present review focused primarily on elucidating the intricate metabolic pathways that underlie macrophage functionality. Subsequently, it offers a comprehensive overview of the current state­of­the­art nanomaterials, highlighting their promising potential in modulating macrophage metabolism to effectively hinder disease progression in both cancer and atherosclerosis.

Electrocatalytic NAD+ reduction via hydrogen atom-coupled electron transfer.

Nicotinamide adenine dinucleotide cofactor (NAD(P)H) is regarded as an important energy carrier and charge transfer mediator. Enzyme-catalyzed NADPH production in natural photosynthesis proceeds via a hydride transfer mechanism. Selective and effective regeneration of NAD(P)H from its oxidized form by artificial catalysts remains challenging due to the formation of byproducts. Herein, electrocatalytic NADH regeneration and the reaction mechanism on metal and carbon electrodes are studied. We find that the selectivity of bioactive 1,4-NADH is relatively high on Cu, Fe, and Co electrodes without forming commonly reported NAD2 byproducts. In contrast, more NAD2 side product is formed with the carbon electrode. ADP-ribose is confirmed to be a side product caused by the fragmentation reaction of NAD+. Based on H/D isotope effects and electron paramagnetic resonance analysis, it is proposed that the formation of NADH on these metal electrodes proceeds via a hydrogen atom-coupled electron transfer (HadCET) mechanism, in contrast to the direct electron-transfer and NAD˙ radical pathway on carbon electrodes, which leads to more by-product, NAD2. This work sheds light on the mechanism of electrocatalytic NADH regeneration, which is different from biocatalysis.