For most people, a sun tan is a synonym of health and beauty. It has not been always like that, however. Since ancient times the idea of human beauty was a snow-white complexion.
Only in the 1920s did people start perceiving sun tan in another way. However, it quickly became clear that an excessive exposure to the sun results in irreversible effects. UltraViolet Radiation (UVR) is a major environmental risk factor that contributes to carcinogenesis through DNA damage and immune modulation via inflammatory and immunosuppressive pathways.1
Darkened skin colour, the result of increased and redistributed epidermal melanin, is a familiar and well-studied response of normal skin to ultraviolet irradiation in humans. This tanning response has been shown to have two distinct phases termed immediate pigment darkening and delayed tanning.2 Both components have strong genetic determinants and are generally far more pronounced in individuals with dark baseline (constitutive) pigmentation. Like all photobiologic responses, tanning requires direct interaction of UV photons with molecular targets in the skin. UVR directly affects epidermal melanocytes, the neural crest-derived skin cells responsible for melanin pigment production, skin pigmentation being considered as a natural protection against environmental insults. UV-induced melanogenesis also involves other cell types, among which keratinocytes appear to play the predominant role, secreting paracrine factors that enhance melanocyte survival, proliferation, dendricity and melanin synthesis. Keratinocytes also accept transferred melanin from melanocytes and thus the pigment is distributed more widely within the epidermis, increasing its photoprotective capacity.3
Tyrosinase, a glycoprotein localised to the melanosome, is the principal and ratelimiting enzyme in melanin synthesis by virtue of its ability to catalyse tyrosine hydroxylation, the first reaction in the biosynthetic sequence. Several other enzymes are known to participate in melanin biosynthesis. These include tyrosinase-related proteins 1 and 2 (TRP1 and TRP2) and melanogenic inhibitors.4
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