Nicotinamide (NSC 13128, Niacinamide, Vitamin PP, Nicotinic acid amide, Vitamin B3, NSC 27452), a water-soluble vitamin, is an active component of coenzymes NAD and NADP, and also act as an inhibitor of sirtuins.
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Nicotinamide (NSC 13128) Nicotinamide (NSC 13128, Niacinamide, Vitamin PP, Nicotinic acid amide, Vitamin B3, NSC 27452), a water-soluble vitamin, is an active component of coenzymes NAD and NADP, and also act as an inhibitor of sirtuins . In vitro
Nicotinamide strongly inhibits yeast silencing, increases rDNA recombination, and shortens replicative life span to that of a sir2 mutant. Nicotinamide abolishes silencing and leads to an eventual delocalization of Sir2 even in G(1)-arrested cells, demonstrating that silent heterochromatin requires continual Sir2 activity. Nicotinamide results in a twofold increase in DNA content and a threefold increase in insulin content in the fetal cells. Nicotinamide induces differentiation and maturation of human fetal pancreatic islet cells. Nicotinamide regulates sirtuins by switching between deacetylation and base exchange. Nicotinamide switching is quantitated for the Sir2s from Archeaglobus fulgidus (Sir2Af2), Saccharomyces cerevisiae (Sir2p), and mouse (Sir2alpha). Nicotinamide selectively reduces a specific phospho-species of tau (Thr231) that is associated with microtubule depolymerization in Alzheimer\'s disease transgenic mice, in a manner similar to inhibition of SirT1. Nicotinamide also dramatically increases acetylated alpha-tubulin, a primary substrate of SirT2, and MAP2c in Alzheimer\'s disease transgenic mice, both of which are linked to increased microtubule stability. Nicotinamide fosters DNA integrity and maintains phosphatidylserine membrane asymmetry to prevent cellular inflammation, cellular phagocytosis and vascular thrombosis. Nicotinamide both prevents and reverses neuronal and vascular cell injury.
In vivo
In the mouse, nicotinamide given i.p. at doses of 100-500 mg/kg showed biphasic elimination with dose-dependent changes in half-life. The initial half-life increased significantly (P <0.05) from 0.8 to 2 h and the terminal half-life increased from 3.4 to 5.6 h over the dose range studied. Clearance, however, decreased significantly from 0.3 to 0.24 L/kg/h only at the highest dose. Peak concentrations increased in a dose-dependent manner from 1,000 to 4,800 nmol/ml. The bioavailability given via the i.p. as compared with the i. v. route was close to 100%. Cell Data
