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Melanin is a brown-black pigment synthesized by melanocytes from tyrosine.

In humans, and in lower animals (the ink of cuttlefish and the cutaneous pigment cells of some animals), melanin serves a protective function.

The skin of individuals adapted to long exposure to sunlight contains much more melanin than does the skin of those living in northern latitudes where such exposure is much less.

This is believed to be an important factor in the widely differing incidences of skin cancers in these two population groups.

Skin cancer, which is virtually unknown among blacks is a very common neoplasm in fair-skin whites.

Measurements of sheets of stratum corneum for their effectiveness in screening out ultraviolet light have shown that such material derived from blacks is much more effective than that from less pigmented people.

Ultraviolet radiation, which stimulates synthesis of melanin, is also highly absorbed by the pigment as part of the protective mechanism.

In addition, since melanin's properties indicate that it is a stable free radical and that its free-radical content increases after exposure to ultraviolet radiation, it may protect by capturing injurious free radicals formed by the action of ultraviolet rays on skin.

Melanin is formed by the oxidation of tyrosine to dihydroxyphenylalanine (dopa), a reaction catalyzed by tyrosinase, a copper-containing enzyme.

Dopa is further oxidized to indole-5,6 -quinone (dopachrome), which in turn is converted by oxidation-reduction to 5,6 -dihydroxyindole, which is polymerized to a highly insoluble substance.

A generalized increase in skin melanin commonly occurs with continued exposure to sunlight, more rarely it is seen in persons with Addison's disease, an adrenocortical insufficiency resulting from destruction of the adrenal cortex.

The mechanism by which melanogenesis is simulated in such cases is an interesting facet of comparative endocrinology.

In the lower animals, melanin formation is under control of a polypeptide hormone called melanin-stimulating hormone (MSH), which is localized in the pars intermedia of the pituitary.

Its existence has not been unequivocally established in humans, in whom melanogenesis appears to be stimulated by adrenocorticotropic hormone (ACTH).

The loss of adrenocortical hormones in Addison"s disease leads to a loss of feedback control of ACTH secretion and so it continues to be secreted at high levels.

The melanin-stimulating properties of ACTH are no doubt related to the fact that a segment of the molecule bears a strong chemical homology to MSH through an identical amino acid sequence.

Increased melanogenesis is also seen in patients with proliferative lesions of melanocytes.

The benign form includes the commonly occurring "pigmented moles" (nevi).

The malignant equivalent, malignant melanoma, is a highly malignant neoplasm that invades normal tissues early and widely and that almost invariably terminates in death.

Such tumours are highly pigmented because of the synthesis of excessive amounts of melanin, which may accumulate in serum and urine, making them gray to black.

An interesting although less common variant is the so-called amelanotic melanoma, in which the neoplastic melanocytes have lost their capacity to produce melanin pigment because of the deletion of one or more of the enzymes necessary for its synthesis.

Albinism is an inherited disorder of melanin metabolism in which there is a decrease or absence of the pigment in the skin and choroid of the eye.It occurs in both lower animals and mammals, including humans.

Careful histologic and ultrastructural studies of the skin of albinos have definitely established that, although melanocytes are present and show an essentially normal structure and complement of cell organelles, including premelanosomes, the latter are devoid of melanin.

The condition may be diffuse, involving all the skin, the eyes, and the hair, or it may be localized to a certain site or sites (piebalding).

Such curious distributions are attributed to the fact that the genetic defect is limited to only a specific group or groups of precursor melanocytes that migrate during embryonic development from the neural crest to peripheral sites where albinism is localized.

Patients with oculocutaneous albinism have poor vision and severe photophobia. The hair is blond. Often with a slight reddish cast, and the skin is exquisitely sensitive to sunlight, becoming rapidly erythematous on exposure.

Chronic exposure invariably leads to the development of precancerous lesions of the skin that ultimately evolve into squamous and basal cell cancers.

A melanin-like pigment is produced in large amounts in alkaptonuria, a rare metabolic disorder involving abnormal metabolism of homogentisic acid, an intermediate product formed in the metabolism of phenylalanine and tyrosine.

The metabolic block is caused by the lack of homogentisic acid oxidase, an enzyme that converts homogentisic acid to methylacetoacetic acid.

The black pigment, a polymer derived from homogentisic acid, accumulates in the skin and connective tissues, specially cartilage of the nose, ears, ribs, joints, and the tendons of the hands, such pigmentation is referred to as ochronosis.

The pigment also appears in perspiration and is excreted in the urine.