Study Finds Protecting Skin Cells from UV Damage Depends on NMN Synthesis

Our cells depend on nicotinamide adenine dinucleotide (NAD+) to function and survive. Drops in NAD+ levels caused by aging are linked to diseases like metabolic disorders, cancer, and neurodegenerative conditions. Similar to aging, harmful UV rays from the sun can also trigger NAD+ depletion. Understanding how these NAD+ depleting phenomena work and can be prevented or reversed has become a hot topic in research. 

Tsuji-Naito and colleagues from the DHC Corporation Laboratories in Japan published a study in the Journal of Photochemistry and Photobiology showing that UV damage activates NAD+ synthesis and NAD+ consuming enzymes in a balancing act that determines survival or dysfunction for human skin cells. They show that, in a tug of war, UV radiation activates nicotinamide phosphoribosyltransferase (NAMPT) to produce the NAD+ precursor nicotinamide mononucleotide (NMN) and also activates the NAD+ consuming enzyme poly ADP-ribose polymerase (PARP). If NAD+ synthesis falters during this balancing act, PARP will severely deplete NAD+ levels, which can trigger skin cell proliferation arrest and dysfunction. Interestingly, blocking NAMPT’s NAD+ production lets PARP drain NAD+, but supplementing with the NAD+ precursors NMN (100 µM) or nicotinamide riboside (NR; 50 µM) restores the cells’ abilities to recover from UV damage.

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