In the fight against ageing, there is a new kid on the block: DNA repair. DNA, stored in cells’ nuclei and mitochondria, is the building block of life. The DNA code exists in every single cell in our body, and is responsible for the creation of new cells. Dermatologists all agree: if we don’t protect our DNA, we age faster.
Much like photocopying, if your original DNA code is damaged it will make bad copies of itself, meaning that your cells will not function properly. Skin cells are some of the most rapidly dividing cells in the body, so protecting our DNA from further damage and repairing the damage already caused are the new holy grails in the fight against skin ageing. A host of new products with specific actives to protect DNA are being launched and are becoming as important as antioxidants, anti-inflammatory actives, and peptides.
How does DNA affect our skin?
There are three main factors that cause our skin to age: inflammation, DNA damage, and oxidation. When we talk about DNA damage, it’s important to say that every cell is equipped with a natural repair process, which is switched on and works 24 hours per day. However, some degree of DNA damage can’t be repaired by itself; skin affected with diseases such as cancer has a faulty repair mechanism that makes the process even more difficult, introducing mutations during cell reproduction.
The most common DNA damage is a single strand break, and occurs naturally with normal skin ageing. But double strand breaks, which occur with ultraviolet (UV) radiation or some foreign chemicals, are harder to repair.
Starting at 30 years of age, the DNA repairing process begins to slow down. When the normal repair mechanisms for DNA repair are overrun by the amount of DNA damage, we rapidly see the effects of this manifested as skin wrinkles, skin laxity, and dryness. As DNA damage accumulates with age, the rapid replication of skin cells causes them to be intrinsically vulnerable to replicative senescence, especially if efforts to protect skin cells from damage are not taken. This growing amount of DNA damage is not healthy.
So the secret is to slow the damage rates that occur in our skin — even when we are in our 20s and early 30s. The less our skin’s DNA has been damaged, the better it will look and the healthier it will be; rendering it more able to fight skin cancer and age-related pigmentation changes.
Damage to skin cell DNA can be caused by lifestyle and environmental factors, with UV radiation having the most significant effects. UV radiation can damage DNA through two different mechanisms:
- It directly damages DNA through the absorption of UV light that causes lesions in the DNA chain
- It induces the production of reactive oxygen species (ROS) and advanced glycation end-products (AGEs) that cause damage to DNA.
Direct absorption of UV, primarily UVB, can lead to the production of dimers or lesions. This affects the pyrimidine nucleic acid bases (thymine and cytosine), and leads to the formation of cyclobutane pyrimidine dimers and pyrimidine (6–4) pyrimidone compounds. Purine dimers can also form (between adenine bases and adenine-thymine base interactions) but these are much less common1.
UVA and UVB have different effects on our DNA. UVB — which is absorbed in the epidermis — create DNA lesions. If the damage exceeds the cell’s repair capacities, it leads to cell death and mutation (skin cancer). UVA—which is absorbed in the dermis—also causes DNA damage by oxidation, resulting in skin ageing. UVB also causes DNA damage indirectly. Even though UVB only reaches the epidermis, it causes inflammation, which can further damage the deeper layers of the dermis.
Indirect DNA damage caused by ROS can also cause lesions within a DNA strand. These are usually modifications affecting single bases; the main DNA product generated by the ROS superoxide is 8-hydroxyguanine (8-OHdG) owing to guanine’s low ionising potential, with adenine being the second most susceptible base to oxidation. Pyrimidine glycols such as 5,6-dihydroxydihydrothymine can also be produced2.
Although many physicians assert that the types of DNA lesions formed are the same, it’s important to say that DNA damage occurs in the cells at two places. First in the nucleus — the cell’s control centre — and then in the mitochondria — its energy factory. With damage to both of these centres, the cell is unable to produce the proteins to keep itself healthy, as well as rendering it unable to produce the energy necessary to keep the nucleus functioning optimally to manufacture the essential building blocks (in this case collagen, elastin and hyaluronic acids), as well as new skin cells.
DNA damage also plays a role in melanocytes
DNA damage and an impaired ability for self-repair is greatest in melanocyte cells. Melanocytes are the cells that experience the greatest amount of UV damage and their ability for self-repair is impaired. Although it’s hard to find an explanation for this reduced DNA repair ability there is plenty of evidence. It also explains why melanoma is one of the three main types of skin cancer seen in humans.
Data from a study carried out at NYU School of Medicine showed that melanocytes were more vulnerable to UVA radiation than other skin cells because they were unable to repair their damaged DNA as efficiently3. The irradiated melanocytes showed a higher frequency of mutation, potentially leading to the development of melanoma. In the study, melanocytes exposed to UVA radiation were unable to repair the damage that was detected within their DNA. The authors concluded that UVA-induced oxidative DNA damage in melanocytes and the inherently reduced repair capacity in these cells are the two key factors that contribute to melanoma on the skin.