Upon exposure to UV radiation, DNA damage triggers cytokines, growth factors and other inflammatory factors to stimulate melanin production.
Upon exposure to UV radiation, DNA damage triggers cytokines, growth factors and other inflammatory factors to stimulate melanin production. Melanin forms in specialized cells called melanocytes. Melanocytes are especially abundant in the basal layer of the epidermis and underlying dermis and are responsible for the pigmentation of the skin. The melanocytes, by increasing the production of intracellular nitric oxide (NO), they trigger signal transduction cascades to initiate melanogenesis through a series of oxidative reactions involving the amino acid tyrosine in the presence of the enzyme tyrosinase. This leads to the production of melanin. Melanin granules synthesized in the melanocytes are then transferred from the cytoplasm of the melanocytes to the basal cytoplasm of the keratinocytes. In the human epidermis, melanocytes work in close harmony with their neighbouring cells such as keratinocytes via their dendrites. They thus form a protective covering in the inner layers of the epidermis, absorbing UV rays and inhibiting their penetration.
Initial melanin synthesis is catalyzed by tyrosinase and then divided into eumelanogenesis or pheomelanogenesis. The other melanogenic enzymes, such as, L-3,4-dihydroxyphenylalanine (DOPA), chrome tautomerase (DCT) and tyrosinase-related protein 1 (TYRP1), are involved in eumelanogenesis, and no specific enzymes have been found that are involved in pheomelanogenesis so far.
Tyrosine is oxidised to DOPA which is then converted to dopaquinone, due to the action of tyrosinase. The reaction progress by autoxidation is thought to be accelerated by the enzymes. Tyrosinase also accelerates the reaction of monomer aggregation which leads to the production of eumelanin.