The stratum basale layer of the epidermis, hair, and iris contain a type of cells with the ability to produce melanin for the human body, which are known as melanocytes. Melanocytes are derived from embryonic cells and neural crest cells (NCC), and undergo several life cycles involving melanocyte differentiation from NCC into melanoblasts, the precursor cells. Melanocytes are reported to migrations and proliferations to the target site, differentiations and maturations into melanocytes, transportations and releases of melanosomes filled with melanin to keratinocytes, and cell death . The skin suffers some stresses such as inflammation and free radical accumulation, especially the UV effect on melanin production for defense against injury from the external or internal environment . Melanogenesis is a complex mechanism and process involving intercommunication between melanocytes, keratinocytes, and fibroblasts, thereby regulating signal transduction by secreting paracrine factors and cytokines. There are numerous paracrine factors which regulate melanin production, such as the proopiomelanocortin (POMC)-derived hormone, [(α-MSH and adrenocorticotropic hormone (ACTH)], ET-1, HGF, CRH, nitric oxide, and some inflammatory cytokines (IL-1β, -6, and -10, and TNF-α) . Most paracrine factors modulate melanogenesis by upregulating or downregulating the expression of the microphthalmia-associated transcription factor (MITF), which ultimately is the primary transcription factor for tyrosinase, tyrosinase-related protein-1 (TRP-1), and dopachrome tautomerase (tyrosinase related protein-2, TRP-2). Melanin synthesis is accompanied by melanosome maturation, the special cellular organelles in melanocytes. Tyrosinase plays a role as a central and rate-limiting enzyme because it initiates the reaction of tyrosine hydroxylation to L-3,4-dihydroxyphenylalanine (L-DOPA) and oxidization into DOPA quinone. In the presence of thiols such as cysteine or glutathione, DOPA quinone reacts with it and generates cysteinyl-DOPA, turning it into yellow-red pheomelanin. On the other hand, spontaneous cyclization of DOPA quinone to DOPA chrome occurs, followed by a spontaneous loss of carboxylic acid to form 5,6-dihydroxyindole (DHI). The dark-brown eumelanin is converted into indole-5,6-quinone by DHI oxidization via TRP-1 and polymerization. If the DOPA chrome is catalyzed by TRP-2 to DHI-2-carboxylic acid and then oxidized to form indole-5,6-quinone-2-carboxylic acid, its polymerization results in lighter brown eumelanin . The final step of skin pigmentation is the transport of mature melanosomes from melanocytes along with cytoskeletal elements to dendrites, followed by internalization by adjacent keratinocytes contacting with melanocytes , and 30–40 associated keratinocytes. The mature melanosomes are transported to the adjacent .