We all know that when we sunbathe, we get a tan, we get freckles or, in the worst case, we get burnt but, what happens in our cells when these events occur?
As we explained in previous posts, cells in our skin are dynamic. This means that they are able to receive information from the surrounding environment and elaborate an adaptation response without stopping their main function. A good example of this adaptation ability occurs when we are exposed to sun light. The ultraviolet (UV) radiation emitted by the sun penetrates our skin and can cause acute damages in our cells. To avoid this, some cells in the epidermis, named melanocytes, mediate a response to this aggression by synthesizing melanin.
Melanocytes are spread all around the skin surface, although not regularly. Some areas, such as the face or genital organs, have a higher proportion of melanocytes than the hands or the trunk. This kind of cells can also be found in other organs such as the heart or the cornea (1). Despite being the main producers of all the melanin in the skin, melanocytes count only 1% of all cells forming the epidermis (2). As it has been mentioned before, their main function is to produce melanin in a synthesis process regulated by genetic factors, hormonal changes and external agents (such as UV radiation).
UV radiation induces the activation of transcription factors in the melanocytes, which function as a starting signal for the synthesis of melanin. Once this polymer is produced, it is “packaged” in spherical molecules, named melanosomes, which are transferred to other epidermal cells: the keratinocytes (5). Each melanocyte is surrounded by roughly 30-40 keratinocytes, which enables an efficient transference of melanosomes between them (6). Melanosomes accumulated in the keratinocytes from the outermost layers of the epidermis are responsible for the skin tone.
What is melanin?
Melanin is a polymer, derived from the amino acid tyrosine, responsible for the skin and hair pigmentation in humans and other animals. There are three kinds of melanin (3):
- Eumelanin: black/brown pigment that confers a dark coloration.
- Pheomelanin: yellow/red pigment that confers a lighter coloration.
- Neuromelanin: dark pigment found in the brain. It tends to accumulate with age. Its function is not fully elucidated and could be implicated in the development of Parkinson’s disease (4).
However, UV radiation arriving in the Earth surface from the Sun could be of two kinds: UVA and UVB, and each one influences melanin synthesis in a different way. UVA radiation can oxidize melanin already present in keratinocytes resulting in an immediate skin darkening. In contrast, UVB radiation activates the melanin synthesis in the melanocytes. For a period of 4/5 weeks, melanocytes increase the melanin production and the packaging density in the melanosomes. If radiation exposure continues, melanocytes start to divide amplifying their population up to 3-4 times, which in turn, promotes a significant increase in melanin synthesis. All these events result in high levels of melanin in the epidermis and the consequent long-term skin darkening, or suntanned, as it is usually recognized. If sun exposure stops, melanosomes degrade as keratinocytes move towards the outermost layers of the skin. That is why suntanned acquired during summertime is usually lost in winter (7).
Melanin functions as a protector substance for our body since, thanks to its dark color, it is able to absorb UV radiation which, if absorbed by other molecules could result highly harmful. Moreover, melanin has an antioxidant effect that can minimize the toxicity of free radicals generated by UV radiation and be potentially harmful for our cells (2).
Thus, in normal conditions, melanocytes are the cells in charge of protecting our body from sun radiation and the so desired tanning is the procedure by which our body defends from sun damage.
Nevertheless, when sun exposure is continued or when UV radiation is too high, melanin cannot absorb it all and some is collected by other molecules such as DNA, lipids or proteins, which are seriously damaged. Our body, in order to avoid that these effects get worse, produces an inflammation in the affected area visible by the red color the skin acquires when we usually say we are sunburned (8).
REFERENCES
- Yamaguchi Y, Hearing VJ. Melanocytes and their diseases. Cold Spring Harb Perspect Med. 2014;4(5).
- Brenner M, Hearing VJ. The protective role of melanin against UV damage in human skin. Photochem Photobiol. 2008;84(3):539–549.
- Kondo T, Hearing VJ. Update on the regulation of mammalian melanocyte function and skin pigmentation. Expert Rev Dermatol. 2011;6(1):97–108.
- Martin-Bastida A, Pietracupa S, Piccini P. Neuromelanin in parkinsonian disorders: an update. Int J Neurosci. 2017 Dec;127(12):1116-1123.
- Maranduca MA, Branisteanu D, Serban DN, et al. Synthesis and physiological implications of melanic pigments. Oncol Lett. 2019;17(5):4183–4187.
- Cichorek M, Wachulska M, Stasiewicz A, Tymińska A. Skin melanocytes: biology and development. Postepy Dermatol Alergol. 2013;30(1):30–41.
- Lambert MW, Maddukuri S, Karanfilian KM, Elias ML, Lambert WC. The physiology of melanin deposition in health and disease. Clin Dermatol. 2019 Sep -Oct;37(5):402-417.
- Young AR, Chadwick CA, Harrison GI, Nikaido O, Ramsden J, Potten CS. The similarity of action spectra for thymine dimers in human epidermis and erythema suggests that DNA is the chromophore for erythema. J Invest Dermatol. 1998 Dec;111(6):982-8.
