Ensuring Skin Cell Resilience Against UV Harm Hinges on NMN Production: New Research Findings
Nicotinamide adenine dinucleotide (NAD+) plays a pivotal role in cellular function and survival. Aging-induced NAD+ depletion is connected to various ailments, such as metabolic diseases, cancer, and neurodegenerative disorders. Similarly, harmful UV sunlight can also induce NAD+ depletion. As such, the mechanisms underlying these NAD+ depletion scenarios and their potential prevention or reversal have garnered significant attention in scientific research.
Study Findings on UV Damage and NAD+ Synthesis
A study carried out by Tsuji-Naito and colleagues from DHC Corporation Laboratories in Japan, published in the Journal of Photochemistry and Photobiology, unveiled that UV damage instigates a balance between NAD+ synthesis and consumption that influences the fate of human skin cells. The study found that UV light triggers the NAD+ precursor-creating enzyme, nicotinamide phosphoribosyltransferase (NAMPT), and the NAD+ consuming enzyme, poly ADP-ribose polymerase (PARP). If the balance shifts and NAD+ synthesis decreases, PARP drastically reduces NAD+ levels, leading to potential skin cell proliferation halt and dysfunction.
Understanding NAMPT’s Protective Role
"Understanding NAMPT's protective role against UV stress could help in preventing and treating skin photoaging," commented Tsuji-Naito and colleagues. NAMPT contributes to cell health and viability by generating NAD+ precursor, NMN. The team found that inhibiting NAMPT led to a severe shortage of NAD+ in UV-irradiated cells, confirming its crucial role in maintaining NAD+ levels to counteract PARP.
The Effects of UV Rays on NAMPT and PARP
Further investigations revealed that UV light exposure increased NAMPT activity almost threefold, driving cell energy production in response to UV damage. However, inhibiting NAMPT during UV exposure resulted in a roughly 35% reduction in cell survival, highlighting NAMPT's role in promoting cell health post-UV damage.
In contrast, the PARP enzyme is vital for DNA repair and cellular survival but consumes vast amounts of NAD+ in the process. UV light can stimulate PARP, potentially due to UV-induced DNA damage. Tsuji-Naito's team discovered that PARP activation significantly contributes to the decrease in NAD+ levels in UV-exposed skin cells.
NAD+-Boosting Molecules: A Solution to Skin Aging?
The findings suggest a delicate balance between PARP, which consumes NAD+, and NAMPT, which produces NAD+ under UV exposure. As age progresses, this equilibrium can deteriorate, predisposing individuals to age-related conditions. Remarkably, supplementing UV-damaged skin cells with NMN or NR during NAMPT inhibition restored cellular energy production and proliferation, indicating these NAD+-enhancing molecules might help maintain NAD+ balance during UV damage and skin aging.
Conclusion
Tsuji-Naito and colleagues concluded, "Our research not only clarifies NAMPT's role in protecting the skin against daily UVA/B exposure, but it also identifies NMN and NR as potential therapeutic agents for age-related skin conditions and functional decline."
The study elucidates the intricate dynamics of maintaining NAD+ levels as we age. For instance, diminished NAMPT enzyme levels could lead to drastic NAD+ depletion due to increased PARP consumption, particularly under UV skin damage. Importantly, the research also supports that augmenting NAD+ levels with supplements like NMN or NR can enhance skin cell health during aging. This knowledge could also facilitate the development of innovative methods to prevent age-related skin damage.