• NMN reduces harmful molecules called reactive oxygen species (ROS) in human skin cells exposed to particulate matter. 
  • Senescent (aged) cells are elevated in response to particulate matter exposure but reduced by NMN. 
  • Treatment with NMN also reduces markers of inflammation and increases levels of the longevity-associated enzyme sirtuin 1.

Whether indoors or outside, chances are you are surrounded by particulate matter (PM) — harmful microscopic matter suspended in the air. These tiny particles, invisible to the naked eye, are not only dangerous if inhaled but also contribute to skin aging. Now, researchers from Hungkuang University and China Medical University in Taiwan may have found a way to limit the harmful effects of PM on our skin.  

As reported in the International Journal of Molecular Sciences, Chang and colleagues use two naturally occurring molecules important for cellular energy production — nicotinamide mononucleotide (NMN) and coenzyme Q10 (Q10) — to protect skin cells from PM-induced skin aging. They show that human skin cells exposed to PM have increased levels of ROS and senescent cells. Both ROS and senescent cells were reduced by NMN, while only senescent cells were reduced by Q10. The Taiwanese researchers also show that inflammatory markers are reduced by NMN and Q10, while the longevity-associated enzyme sirtuin 1 is increased. 

NMN Alleviates Particulate-Matter Induced Skin Aging

To study the effect of NMN and Q10 on PM-induced skin aging, Chang and colleagues exposed human skin cells to PM and then treated them with NMN or Q10. They found that skin cells exposed to PM had increased levels of ROS, molecules that can cause damage to cells. Treating PM-exposed skin cells with NMN lowered ROS levels, suggesting NMN reduces oxidative stress — damage caused to cells by ROS. 

(Chang et al., 2022 | Int. J. Mol. Sci.) NMN Reduces Particulate Matter-Induced Reactive Oxygen Species (ROS). Human skin cells exposed to PM (PCM) have higher levels of ROS (measured by DCFH-DA fluorescence) than unexposed (control) skin cells. These ROS were reduced by NMN but not Q10.

As we age, our cells encounter cellular stressors such as oxidative stress, inflammation, and DNA damage. Cellular stress can cause our cells to go into a senescent state, whereby the affected cells no longer divide but promote inflammation, contributing to age-related disease. When Chang and colleagues exposed human skin cells to PM, they saw an increase in senescent cells. By treating the skin cells with either NMN or Q10, the number of senescent cells was reduced. 

(Chang et al., 2022 | Int. J. Mol. Sci.) NMN Reduces Particulate Matter-Induced Senescent Cells. Human skin cells exposed to PM (PCM) have more senescent cells (measured by β-gal) than unexposed (control) skin cells. These senescent cells were reduced by both NMN and Q10.

Examination of PM-exposed skin cells revealed elevated levels of inflammatory markers, which Chang and colleagues showed were counteracted by both NMN and Q10 treatment. Additionally, the longevity-associated enzyme sirtuin 1 (SIRT1) was suppressed in PM-exposed skin cells. However, NMN and Q10 restored this important DNA-repairing enzyme. These findings suggest that NMN and Q10 protect the skin against PM-induced inflammation and potential DNA damage. Furthermore, NMN showed much stronger effects in comparison to Q10.

Protecting Ourselves Against Particulate Matter-Induced Aging

Studies have shown that long-term exposure to PM is associated with an increased risk of death and all diseases worldwide. Additionally, air pollution, which contains some of the most dangerous levels of PM, is associated with age-related conditions like olfactory decline, cognitive decline, osteoporosis, cardiovascular disease, and lung cancer

NMN is an intermediate molecule used by our cells to make nicotinamide adenine dinucleotide (NAD+), which SIRT1 uses as fuel. In turn, SIRT1 prevents cellular senescence and protects against oxidative stress and DNA damage. Like Q10, NAD+ is also an important mediator of energy production and mitochondrial function. So, by boosting NAD+, can NMN protect our skin from PM and stop premature skin aging?

Similar to the findings of Chang and colleagues, researchers have recently shown that, in human skin cells, a combination of ultraviolet (UV) radiation and PM induces high levels of ROS, inflammation, and senescent cells. These aging markers were reduced by a vitamin C and E compound. Similarly, NMN has been shown to protect skin against UV damage in mice. Another recent study showed that PM promotes the production of skin melanin, which can be reduced by NMN in rodents.

Overall, while there is plenty of research to suggest that PM causes accelerated aging of the skin and other organs, there is limited research investigating how to protect against PM. Given the evidence, the next questions is whether topical application of NMN can protect the skin against aging in humans, as previous studies have shown that non-topical administration of NMN does so in animal models.