Prolonged sunlight exposure can be harmful for our skin, leading to premature aging and potential cancer development. Now, scientists show that sunlight can still damage skin in the dark, long after sunlight exposure has ended.
Sunlight is beneficial for human health, mostly because of it’s ability to boost Vitamin D, a vitamin important for a number of significant functions like bone formation and proper functioning of the neuromuscular and immune system. However, too much sun exposure can be harmful for our skin, leading to premature aging by reducing skin elasticity and increasing our risk for skin cancer development.
Melanin, our protector against sunlight induced skin damage
The skin’s natural defense against sun damage is the pigment melanin, produced by cells called melanocytes. When we are exposed to sunlight, melanocytes increase their melanin production, causing skin to darken. Increased production of melanin shields our skin from harmful ultraviolet (UV) rays by forming a physical barrier that scatters the rays and prevents them from penetrating the inner layers of our skin. The protective effect of melanin is demonstrated by the fact that people with lighter skin are 70% more likely to develop skin cancer than people with naturally darker skin.
The nasty side of melanin
However, recent research shows that there may also be a nasty side to melanin. According to a study published in Science by Douglas Brash and colleagues at Yale University School of Medicine New Haven, Connecticut, it now appears that sunlight can still damage our skin long after actual sunlight exposure. The surprising culprit for this effect is melanin, the same pigment that was thought to be protective.
More specifically, when exposing mouse and human melanocytes to UV light, scientists observed that there was increased DNA damage, which they assessed by looking at the levels of production of certain DNA dimers called cyclobutane pyrimidine dimers (CPDs). The DNA damage caused by CPDs, in which two neighboring DNA nucleotides attach and distort DNA, prevent the code it holds from being deciphered properly. This can lead to the production of proteins that don’t function properly.
Generation of CPDs in melanocytes, surprisingly, persisted for up to three hours after UV light exposure had come to an end. These ‘dark’ CPDs seemed to arise when UV-induced reactive oxygen and nitrogen species combined to excite an electron in the pigment melanin. The energy created from this process was responsible for the DNA damage caused in the dark.
The results from this study show a dual role for melanin. On the one hand it acts as a skin protector, by forming a natural barrier that prevents harmful rays from entering the inner layers of our skin. On the other hand, it provides a molecule that, upon excitement, fuels the generation of damaging CPDs even long after exposure to sunlight has ended.
Can the damaging effect of melanin be counteracted?
Searching for a way to prevent the effect of CPDs on DNA, or reduce CPD generation as an effect of sunlight exposure, scientists observed that treating melanocytes with vitamin E abolished CPD production. This interesting finding could be useful in the development of aftersun sunscreen lotions that can potentially block the carcinogenic effects of sunlight occurring in the dark, even after the end of sunlight exposure.
Science 347, 842–847 (2015)
Photochem Photobiol. 84 (3), 539–549 (2008)