China
Africa
Explore chapters and articles related to this topic
Disorders of Pigmentation
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Michael Joseph Lavery, Charles Cathcart, Hasan Aksoy
Melanin is derived from phenylalanine and passes through several steps before forming pheomelanin, eumelanin, or neuromelanin (Figure 25.1). Pheomelanin produces yellow-red pigment, and eumelanin produces brown-black pigment. The process of determining which pigment is produced is controlled by the melanocortin-1 receptor (MC1R). A loss of function in this receptor leads to increased production of pheomelanin and can increase the risk of melanoma from ultra-violet radiation. Genetic variations in the MC1R gene have been identified in malignant melanoma and oculocutaneous albinism.
The Integumentary (Dermatologic) System and Its Disorders
Published in Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss, Understanding Medical Terms, 2020
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss
Disorders of melanin pigmentation are classified as hypomelanosis (hypo = low, osis = condition; thus, relative lack of melanin) or hypermelanosis (presence of increased melanin). Albinism is an extreme example of hypomelanosis; others include phenylketonuria and vitiligo. Both freckles (ephelides) and moles (nevi) are types of hypermelanosis.
Familial Atypical Multiple Mole Melanoma Syndrome
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
MC1R is a critical player in the pigmentation of human skin. Specifically, it increases the proportion of eumelanin to pheomelanin. Eumelanin is the major workhorse in protecting darker skin from UV damage. Healy et al. found that MC1R contributes to tanning ability in non-red-haired individuals [51]. α-MSH binds to the 7-pass transmembrane protein MC1R, activating adenylate cyclase, and thus increasing cAMP. Increased levels of cAMP trigger expression of microphthalmia transcription factor (MITF), which plays a key role in melanin production. Increased cAMP also leads to the protein kinase A (PKA) phosphorylation of cAMP response-element binding protein (CREB).
Skin impacts from exposure to ultraviolet, visible, infrared, and artificial lights – a review
Published in Journal of Cosmetic and Laser Therapy, 2021
Juliana Yuka Furukawa, Renata Miliani Martinez, Ana Lucía Morocho-Jácome, Thalía Selene Castillo-Gómez, Vecxi Judith Pereda-Contreras, Catarina Rosado, Maria Valéria Robles Velasco, André Rolim Baby
In parallel, there is regulation of skin pigmentation, through melanin, recognized by the skin tanning. The mechanism is divided into two phases: an initial rapid response of distribution and molecular changes in the existing melanin; hours or days after exposure, a delayed response occurs of melanin synthesis with subsequent transfer to keratinocytes. The process begins through hormonal interactions between keratinocytes and melanocytes – after damage caused to the DNA of keratinocytes, there is the production of a pro-opiomelanocortin gene, which stimulates the production and secretion of alpha-melanocyte-stimulating hormone. In this way, the skin is more protected against possible future exposures. Moreover, skin pigmentation depends on the type of skin, which is defined by the proportion of the main chemical structures of melanin: eumelanin and pheomelanin. Such proportion also defines the cutaneous response to UV radiation, as well as cancer risk (13).
Afamelanotide for prevention of phototoxicity in erythropoietic protoporphyria
Published in Expert Review of Clinical Pharmacology, 2021
Debby Wensink, Margreet A.E.M. Wagenmakers, Janneke G. Langendonk
Afamelanotide is a synthetic α-MSH analog. Afamelanotide chemically differs from α-MSH by substitution of the amino acids methionine and L-phenylalanine at positions 4 and 7 with norleucine and D-phenylalanine [Nle4-D-Phe7]-α-MSH. This manipulation of the stereo-chemical structure of α-MSH was performed in order to make afamelanotide more potent and prolong biological activity [54]. Afamelanotide works as an agonist on the MC1R, a G protein-coupled receptor that plays a key role in the biosynthesis of melanin. Binding of afamelanotide to MC1R activates eumelanogenesis, by increasing intracellular content of cyclic AMP (cAMP) and increasing tyrosinase activity, the rate-limiting step in melanogenesis [55]. Afamelanotide acts in the same way as endogenous MSH on MC1R, but independent of UV stimulation. Eumelanin exhibits numerous effects, including photo protection against ultraviolet (UV) light (by absorbing the UV light) and scavenging of free radicals [56].
Synthesis, computational studies, tyrosinase inhibitory kinetics and antimelanogenic activity of hydroxy substituted 2-[(4-acetylphenyl)amino]-2-oxoethyl derivatives
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2019
Muhammad Rafiq, Yasir Nazir, Zaman Ashraf, Hummera Rafique, Samina Afzal, Amara Mumtaz, Mubashir Hassan, Anser Ali, Khurram Afzal, Muhammad Rizwan Yousuf, Muhammad Saleem, Katarzyna Kotwica-Mojzych, Mariusz Mojzych
Melanin is a pigment, primarily responsible for skin colour. It retains antioxidative and photoscreening effect, therefore, provides skin photo-protection, prevents from injury and, absorbs and transforms harmful UV radiations into harmless heat8. Despite its advantages, increased production and accumulation of pigmentations can cause skin problems such as freckles, age spots, post-inflammatory hyperpigmentation, lentigo and melanoma. UV which stimulates melanin synthesis is reported to cause gene mutation, DNA damage, impaired immune system and cancer9. Pigmentation in metastatic melanoma patients results in short overall and disease-free survival10. Melanin content is correlated with higher disease stage and seems to protect malignant melanocytes from chemo-, radio- and photodynamic therapy11,12. Therefore, inhibition of melanogenesis could be a rational approach for controlling metastatic melanoma, abnormal skin pigmentation and related disorders10.