Depigmentation

Copper is required for all forms of aerobic and most forms of anaerobic life. In humans, the biological function of copper is related to the enzymatic action of specific essential copper proteins (66). Lack of these copper enzymes is considered a primary factor in cerebral degeneration, depigmentation, and arterial changes. Because of the abundance of copper in most human diets, chemically significant copper deficiency is extremely rare (67). 

Desalting and depigmentation of urine sample was carried out by gel-filtration on Sephadex G25 with cut mass 10 kDa. 

Dooley TP (1997) Topical skin depigmentation agents current products and discovery of novel inhibitor of melanogenesis. J Dermatol Treat 8 ... 

Skin Poikiloderma Lichen planus-like features Sclerotic features Morphea-1 ike features Lichen sclerosus-like features Depigmentation Seat impairment Ichthyosis Keratosis pilaris Hypopigmentation Hypergimentation Erythema Maculopapular rash Pruritus... 

Adverse effects of copper deficiency can be documented in terrestrial plants and invertebrates, poultry, small laboratory animals, livestock — especially ruminants — and humans. Data are scarce or missing on copper deficiency effects in aquatic plants and animals and in avian and mammalian wildlife. Copper deficiency in sheep, the most sensitive ruminant mammal, is associated with depressed growth, bone disorders, depigmentation of hair or wool, abnormal wool growth, fetal death and resorption, depressed estrous, heart failure, cardiovascular defects, gastrointestinal disturbances, swayback, pathologic lesions, and degeneration of the motor tracts of the spinal cord (NAS 1977). 

Gy LD50, 200 days after exposure skin lesions and depigmentation 5... 

Menter JM, Moore CL, Willis I, Fisher MS. Melanin markedly accelerates the tyrosinase mediated oxidation of phenohc depigmenters. Photochem Photobiol 1986 43 255. 

Bleehan SS, Pathak MA, Hori Y, et al. 1968. Depigmentation of the skin with 4-isopropylcatechol, mercaptoamines and other compounds. J Invest Derm. 50 103ff. 

KahnG. 1970. Depigmentation caused by phenolic detergent germicides. Arch Dermatol 102 177-187. 

McGuire J, Hendee J. 1971. Biochemical basis for depigmentation of skin by phenolic germicides. J Invest Dermatol 57 256-261. 

Zinc deficiency causes growth inhibition, depigmentation of dark hair, balding, corneous and thick epithelium and skin desquamation. Acute deficiencies of zinc lead to testicular atrophy and to sterility (Shils et ah, 1994). 

It is estimated that the average daily tin uptake per adult is approximately 4 mg, however tin is not accumulated in the body. So far, the role of tin in the human body has not been completely understood, although some data lead to the conclusion that it is involved in oxidation-reduction processes. Some authors suggest that the lack of tin in the fodder of test animals causes reduced growth and tooth depigmentation (Schwartz et ah, 1970). 

During the industrial handling of 4-methoxyphenol, two of eight process workers developed skin depigmentation. ... 

Furanocoumarlns have a number of scientifically interesting and even economically and medicinally Important actions. They are effectively used in human medicine in the treatment of vitiligo (skin depigmentation, leukoderma) ( ) and psoriasis (10,11), and have shown promise against certain other human maladies (12-15). Plants that contain furanocoumarlns are known to cause acute photosensltlzatlon (phytophotodermatltls) in man (2,16). 

In a study of intermediate duration, dermal application of 0.5% p-cresol for 6 weeks produced permanent depigmentation of the skin and hair of mice (Shelley 1974). A caustic effect on the skin was noted in one strain of mouse, but not another. Neither o- nor m-cresol produced any color change in the mice. The author suggests that only p-cresol is active because it mimics the structure of tyrosine, the amino acid present in melanin, so that tyrosinase acts on it, liberating free radicals that damage melanocytes. NOAEL and LOAEL values were not derived from this study because the applied dose was not reported. 

Shelley WB. 1974. p-Cresol Cause of ink-induced hair depigmentation in mice. Br J Dermatol 90 169-174. 

The most common adverse effect produced by didanosine is diarrhea. Abdominal pain, nausea, vomiting, anorexia, and dose-related peripheral neuropathy may occur. Pancreatitis occurs rarely, as do hyperuricemia, bone marrow suppression, retinal depigmentation, and optical neuritis. Resistance to didanosine appears to result from mutations different from those responsible for zidovudine resistance. 

Skin depigmentation effect. Extract of the dried seed, administered externally to adults at a dose of 5%, was active. Skin-lightening cosmetics contained extract of Coffea arabica seeds (containing chlorogenic acid) as melanin-formation inhibitors. The extract has been incorporated into cosmetics for skin-aging prevention or into hair preparations for hair protection. Biological activity reported has been patented . 

Pharmacokinetics Onset and duration of depigmentation vary among individuals. About 35% is absorbed. 

Mecfianism of Action The mechanism of action is not fully understood. Monobenzone maybe converted to hydroquinone, which inhibits the enzymatic oxidation of tyrosine to DOPA it may have a direct action on tyrosinase, or it may act as an antioxidant to prevent SH-group oxidation so that more SH groups are available to inhibit tyrosinase. Therapeutic Effect Depigmentation in extensive vitiligo. 

Adverse effects include nausea, vomiting, diarrhoea, anaphylaxis, hepatic necrosis, fever, bone marrow depression, osteoporosis, menstrual dysfunction, cirrhosis, pulmonary infiltrates and fibrosis, renal toxicity and depigmentation. 

Hydroquinone, monobenzone (Benoquin, the monobenzyl ether of hydroquinone), and mequinol (the monomethyl ether of hydroquinone) are used to reduce hyperpigmentation of the skin. Topical hydroquinone and mequinol usually result in temporary lightening, whereas monobenzone causes irreversible depigmentation. 

In Ancient Egypt, there were some recipes for the treahnent of bums either in the critical phase or in the cicatricial phase and particularly a recipe to treat the ugly depigmentation of naturally tanned skins, daily exposed to a strong sun. 

Two genetic disorders of copper metabolism, Wilson s disease (see Section 62.2.3.3) and Menkes disease, are known. The latter involves impaired intestinal absorption of copper56,57 as well as probably subcellular metabolic defects which result in copper deficiency with respect to metal-loenzyme activity. The characteristic steely hair in Menkes disease results from free SH bonds in hair protein because of failure of lysyl oxidase to produce the disulfide links. Depigmentation of hair and skin, hypothermia, cerebral degeneration, central nervous system retardation, skeletal demineralization and arterial degeneration are all seen. Copper supplements may benefit hypothermia and increase pigmentation but the disease is not generally cured. 

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