Skin âcolorâ is determined mainly by the type and amount of melanin deposited in the epidermis. Melanin is a large bio-polymer composed of subunits of different melanotic pigment species formed by sequential oxidation and cyclization of the amino acid tyrosine). Biosynthetic reactions are catalyzed by several pigment enzymes, which when defective, render hypopigmented phenotypes. Tyrosinase is the rate-limiting enzyme that catalyzes the first two steps in melanogenesis, namely conversion of tyrosine into DOPA and then subsequently into DOPAquinone . Loss of function of tyrosinase is the defect in the most common type of human albinism. In the skin, melanin is synthesized in melanocytes and then transferred to keratinocytes where it accumulates to protect the skin against UV injury. There are two basic types of melanin: eumelanin and pheomelanin. Eumelanin is a far better âsunscreenâ than pheomelanin. After a common biosynthetic pathway mediated by tyrosinase, eumelanin and pheomelanin synthesis diverge after the formation of dopaquinone. Eumelanin is preferentially expressed in UV-protected people with dark complexions. It is chemically inert, poorly-soluble and quite efficient at absorbing UV photons. In contrast, pheomelanin is the melanin preferentially expressed in UV-and skin cancer-prone individuals of light complexion. Due to incorporation of cysteine into its precursors, pheomelanin is a red-yellow sulfur-containing compound. UV resistance is mainly determined by the levels of eumelanin found in the epidermis. Besides allowing more UV energy to pass through the superficial layers of the epidermis to cells in the basal layer, pheomelanin may actually contribute to UV-induced free radical formation and oxidative DNA damage in the skin. The contribution of pheomelanin to UV-induced carcinogenesis is an ongoing area of investigation.
Last date updated on March, 2021