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Evidence for epidermal acetylcholine accumulation after oxidative stress by H 2 O 2 and possible implications
Author(s) -
Elwary S.,
Gibbons N.,
Rokos H.,
Wood J. M.,
Schallreuter K. U.
Publication year - 2004
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.0906-6705.2004.0212ce.x
Subject(s) - oxidative stress , acetylcholine , acetylcholinesterase , chemistry , vitiligo , endocrinology , medicine , biochemistry , enzyme , dermatology
Acetylcholine (Ach) has been shown to be synthesized de novo and degraded in the human skin (1), while the presence of acetylcholinesterase (AchE), the degrading enzyme, was first mentioned in 1989 (2). It is now accepted that H 2 O 2 ‐related oxidative stress is a major player in the development/acceleration of vitiligo (3). This oxidative stress affects the recycling of the essential cofactor (6R)‐ l ‐erythro 5,6,7,8 tetrahydrobiopterin (6BH4) via H 2 O 2 ‐mediated oxidation of Trp and Met residues in the structure of pterin‐4a carbinolamine dehydratase (PCD) and dihydropteridine reductase (DHPR) (3). Only very recently, it was recognized that AchE is also affected and deactivated by 10 −3 m H 2 O 2 causing the accumulation of Ach in the epidermis of patients with vitiligo (4). One of the implications of oxidative stress in vitiligo includes pruritus, which was for a long time attributed to the presence of epidermal H 2 O 2 in the 10 −3 m range. In this context, a role for Ach has been suggested in association with pruritus, and therefore, we would like to suggest that Ach accumulation caused by H 2 O 2 ‐mediated deactivation of AchE may well initiate pruritus (5). The Ach accumulation can also explain the earlier documented decreased sweating in patients with vitiligo (6).