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Reduced nicotinamide adenine dinucleotide (NADH) is the reduced form of the essential coenzyme nicotinamide adenine dinucleotide (NAD), playing a fundamental role in cellular energy production [1]. It serves as the primary electron donor for the mitochondrial electron transport chain, specifically at Complex I (NADH:ubiquinone oxidoreductase), which is critical for the generation of adenosine triphosphate (ATP) via oxidative phosphorylation [2]. Beyond energy metabolism, the NAD+/NADH ratio is a key regulator of the cellular redox state and influences pathways such as glycolysis, the citric acid cycle, and DNA repair [3]. Clinical interest in NADH stems from its potential to treat conditions characterized by energy depletion or oxidative stress, including Parkinson's disease, Alzheimer's disease, and chronic fatigue syndrome [4]. As a therapeutic agent, it is often administered as a stabilized oral supplement to boost mitochondrial function and cognitive performance [5].
NADH acts as a biological reducing agent, donating electrons to the mitochondrial respiratory chain (Complex I) to drive ATP synthesis and acting as a cofactor for numerous dehydrogenase enzymes involved in core metabolic pathways [1, 2].
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