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β-Nicotinamide adenine dinucleotide, commonly known as NAD+, is a vital coenzyme found in all living cells that plays a central role in metabolism and cellular physiology. It is a dinucleotide composed of two nucleotides joined through their phosphate groups: one containing an adenine base and the other nicotinamide.

Mechanism of Action

NAD+ primarily functions as an essential coenzyme in redox reactions, acting as an electron carrier. It cycles between an oxidized form (NAD+) and a reduced form (NADH):
Redox Reactions: NAD+ accepts electrons (in the form of a hydride ion) from metabolic substrates during processes like glycolysis, the tricarboxylic acid (TCA) cycle, fatty acid oxidation, and oxidative phosphorylation. This electron transfer is crucial for ATP production and energy metabolism.
Enzymatic Cofactor: NAD+ serves as a cofactor for various dehydrogenase enzymes, facilitating oxidation-reduction reactions essential for cellular respiration and biosynthesis.
Substrate for NAD+-Dependent Enzymes: Beyond redox roles, NAD+ is a substrate for enzymes involved in post-translational modifications, including sirtuins (protein deacetylases), poly(ADP-ribose) polymerases (PARPs), and ADP-ribosyl cyclases, which regulate DNA repair, gene expression, and calcium signaling.
RNA Capping: NAD+ can be incorporated as a non-canonical cap at the 5′ end of RNA transcripts, influencing RNA stability and gene expression regulation.

Biosynthesis and Metabolism

NAD+ levels in cells are maintained through multiple pathways:
De Novo Synthesis: NAD+ can be synthesized from dietary amino acids like tryptophan via the kynurenine pathway.
Preiss-Handler Pathway: Converts dietary nicotinic acid (NA) into NAD+ through intermediate steps.
Salvage Pathway: The predominant pathway in most cells, recycling nicotinamide (NAM), nicotinamide riboside (NR), and nicotinamide mononucleotide (NMN) back into NAD+ to maintain cellular levels. The rate-limiting enzyme in this pathway is nicotinamide phosphoribosyltransferase (NAMPT).
Methylation and Excretion: Excess NAM is methylated by nicotinamide N-methyltransferase (NNMT) and ultimately excreted, regulating NAD+ homeostasis.