Pharmacologic manipulation of skin pigmentation

Abstract

Skin complexion is among the most recognizable phenotypes between individuals and is mainly determined by the amount and type of melanin pigment deposited in the epidermis. Persons with dark skin complexion have more of a brown/black pigment known as eumelanin in their epidermis whereas those with fair skin complexions have less. Epidermal eumelanin acts as a natural sunblock by preventing incoming UV photons from penetrating into the skin and therefore protects against UV mutagenesis. By understanding the signaling pathways and regulation of pigmentation, strategies can be developed to manipulate skin pigmentation to improve UV resistance and to diminish skin cancer risk.

Keywords: cAMP; melanin; melanocortin 1 receptor; melanocyte; pigmentation.

Figure 1.. Overview of Melanogenesis.

Melanin, a bioaggregate of pigmented compounds, is found in two predominant forms, both of which derive from the amino acid tyrosine. Eumelanin is a dark brown/black species that is highly UV protective whereas pheomelanin, as a result of incorporation of a sulfur molecule donated by cysteine, is a reddish/blonde pigment that is less able to block UV photons. Tyrosinase is the rate-limiting enzyme that catalyzes the first two steps in the synthesis of both melanin types, and pigment-diluting phenotypes such as albinism result when tyrosinase or other melanogenic enzymes are defective.