Atomic Ce sites promote a four-electron pathway of Pt as NADH oxidase mimics for in situ coenzyme regeneration

Abstract

Nicotinamide adenine dinucleotide (NAD⁺) is a key coenzyme for human redox reactions, vital for cellular health and metabolic balance. Lots of NAD⁺-dependent redox enzymes, like alcohol dehydrogenase (ADH) and lactate dehydrogenase, can catalyze both forward and reverse reactions. However, substrate accumulation and inadequate NAD⁺ replenishment hinder forward reactions, disrupting the proper metabolism of these substrates. In this work, we reported atomic Ce-doped Pt (Ce₁Pt) nanoparticles with abundant oxygen vacancy sites to boost NADH oxidase (NOX)-like activity for coenzyme regeneration. Mechanistic studies reveal that atomic Ce doping increases electron density of Pt and surface defects, enhancing O₂ adsorption and accelerating the rate-limiting step. Furthermore, Ce₁Pt employs a 4e⁻ pathway for O₂ reduction during NADH oxidation, minimizing toxic H₂O₂ byproducts and improving detection accuracy by reducing oxidative interference. Finally, Ce₁Pt enables NAD⁺ regeneration and substrate metabolism, offering a promising strategy to counteract excessive alcohol intake or lactate accumulation. Through competitive adsorption between the reduced coenzyme NADH of ADH and chromogenic substrates, a microfluidic device integrated with immobilized Ce₁Pt achieves blood alcohol detection with a low limit of detection of 0.012 mM.