Supplementation of nicotinic acid and its derivatives up-regulates cellular NAD+ level rather than nicotinamide derivatives in cultured normal human epidermal keratinocytes

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Abstract
Nicotinamide dinucleotide (NAD+) is an important component for various biological processes in mammalian cells, such as energy production, redox state maintenance, and gene regulation. In most mammalian cells, NAD+ is produced by vitamin B3, including nicotinamide (NAM) and nicotinic acid (NA). Recently, NAD+ up-regulation therapy has attracted attention for suppressing the aging processes, called rejuvenation. Although various enzymes participate in the NAD+ production pathway, some enzymes are lacking in particular cells. Therefore, it is thought that the suitable material for NAD+ production varies with the types of cells. However, the optimization of the NAD+-precursor for use in topical formulations has rarely been considered. In this study, we asked which precursor is suitable for application against human skin keratinocytes. As a result, NA supplementation 1.3-fold up-regulated intracellular NAD+ level significantly, even with a nicotinamide phosphoribosyltransferase inhibitor, FK866, and its metabolites NA mononucleotide also increased NAD+ level by1.5-fold with 100 μM application. Surprisingly, NAM and its derivatives could not up-regulate cellular NAD+ levels in keratinocytes. The NA supplementation also up-regulated mitochondrial superoxide dismutase (SOD2), which indicates the effect for mitochondria. NA also alleviated rotenone-induced mitochondrial ROS accumulation. These results suggest that NA can be used for topical application for skin rejuvenation.

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