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In this work, glucose oxidase (GOx) cross‐linking to a single‐wall carbon nanotubes (SWCNTs)‐poly(ethylenimine) (PEI) matrix is investigated using cyclic voltammetry (CV) for its direct electrochemistry and kinetics with presence of glucose. The electrochemistry of the bound flavin cofactor, flavin adenine dinucleotide (FAD) of the GOx, is impeded by glucose and recovered at absence of glucose, whereas a non‐specific sugar (e. g. sucrose) has no such effect. The Faradaic current of the GOx in CV decreases when the concentration of glucose increases, while the calculated electron transfer (ET) rate constant (k⁰) of the GOx presents a monotonic increment manner up to 144 % at 70 mM glucose concentration vs. absence of glucose in a deaerated electrolyte solution. Thek⁰and Faradaic current changes demonstrate a strong linear relationship to logarithmic value of glucose concentration up to 20 mM. These results suggest that the entrapped GOx, when exposing to glucose, becomes deactivated in the direct electrochemistry. Further mechanistic analysis suggests the ET reaction of GOx shows a responsive correlation to the non‐ergodicity of those active GOx sites. A control experiment using pure FAD immobilized in the matrix doesn't show responses to glucose addition.

 

Atherosclerosis represents an ever-present global concern, as it is a leading cause of cardiovascular disease and an immense public welfare issue. Macrophages play a key role in the onset of the disease state and are popular targets in vascular research and therapeutic treatment. Carbon nanodots (CNDs) represent a type of carbon-based nanomaterial and have garnered attention in recent years for potential in biomedical applications. This investigation serves as a foremost attempt at characterizing the interplay between macrophages and CNDs. We have employed THP-1 monocyte-derived macrophages as our target cell line representing primary macrophages in the human body. Our results showcase that CNDs are non-toxic at a variety of doses. THP-1 monocytes were differentiated into macrophages by treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA) and co-treatment with 0.1 mg/mL CNDs. This co-treatment significantly increased the expression of CD 206 and CD 68 (key receptors involved in phagocytosis) and increased the expression of CCL2 (a monocyte chemoattractant and pro-inflammatory cytokine). The phagocytic activity of THP-1 monocyte-derived macrophages co-treated with 0.1 mg/mL CNDs also showed a significant increase. Furthermore, this study also examined potential entrance routes of CNDs into macrophages. We have demonstrated an inhibition in the uptake of CNDs in macrophages treated with nocodazole (microtubule disruptor), N-phenylanthranilic acid (chloride channel blocker), and mercury chloride (aquaporin channel inhibitor). Collectively, this research provides evidence that CNDs cause functional changes in macrophages and indicates a variety of potential entrance routes.