Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.10.3.1 (tyrosinase)
 9,065 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Erythema dyschromicum perstans (EDP) was first described in 1957, and electron microscopic studies were reported in 1969. Herein, we describe five cases and compare light and electron microscopic findings, direct and indirect immunofluorescence, and dopa-positive melanocyte counts between normal and affected skin. The results indicate that EDP is a clinically characteristic disorder with a lichenoid reaction in its active phase. This lichenoid reaction leads to a pronounced incontinence of pigment and to decreased numbers of melanocytes and of tyrosinase activity in the involved epidermis. These findings support the suggestion that EDP and lichen planus pigmentosus are possible the same entity. Direct inmunofluorescence and fine structural studies show similar findings to lichen plunus. Patients have low-titer antibodies to extranuclear basal cell components.
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PMID:Erythema dyschromicum perstans. 676 58

Here we show that cyclophosphamide induces disruption of follicular melanogenesis, which is characterized by abnormal transfer of pigment granules to ectopic hair bulb locations, extrafollicular melanin incontinence, disordered formation of melanosomes, and inhibition of melanosome transfer into precortical keratinocytes. This is in contrast to dexamethasone-induced termination of follicle melanogenesis, which activates premature but predominantly normal catagen development. Cyclophosphamide-induced pigmentation disruption was accompanied by significant alterations of biochemical and biophysical markers of melanogenesis, compared to control mice treated either with vehicle or with topical dexamethasone. Electron paramagnetic resonance spectroscopy shows a decline in the melanin signal and predominant eumelanin production. Tyrosine hydroxylase activity of tyrosinase and dihydroxyphenylalanine oxidation drop rapidly, while DOPAchrome tautomerase activity increases and dihydroxyindole carboxylic acid conversion factor activity remains unchanged in cyclophosphamide-treated mice compared to controls. These observations emphasize the key role of tyrosinase as opposed to postdihydroxyphenylalanine oxidase steps in normal and pathological termination of melanogenesis and shows that tyrosinase is the most sensitive target of the melanogenic apparatus for pharmacological regulation. Follicle pigmentation recovers only during the subsequent hair cycle, i.e., after a new anagen hair bulb has been constructed, which points to the existence of a relatively chemoresistant melanoblast-like cell population residing in the noncycling part of the hair follicle.
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PMID:Pharmacological disruption of hair follicle pigmentation by cyclophosphamide as a model for studying the melanocyte response to and recovery from cytotoxic drug damage in situ. 875 58