Molecular evidence that halo in Sutton's naevus is not vitiligo.
Both halo naevus and vitiligo are acquired leucodermas of unknown aetiology. To date a significant contribution of oxidative stress through accumulation of hydrogen peroxide (H2O2) has been documented in the pathomechanism of vitiligo but not in halo naevus. Both epidermal pterin-4a-carbinolamine dehydratase (PCD) and catalase are sensitive markers to follow H2O2 concentration-dependent deactivation of these proteins. In situ protein expression of PCD and catalase was examined in full-skin biopsies from skin phototype-matched controls (n=5), untreated and treated vitiligo patients (n=5) and patients with untreated halo naevus in association with vitiligo (n=3). Vitiligo was treated with pseudocatalase (PC-KUS) only. Catalase levels were determined in epidermal suction blister extracts using fast protein liquid chromatography (FPLC). In addition, epidermal H2O2 levels were followed in vivo by Fourier-transform Raman spectroscopy. The results of this study ruled out a contribution of H2O2 in the millimolar range in the depigmentation process of halo naevus as previously documented in vitiligo. Therefore, it can be concluded that both leucodermas exercise distinct concentration-dependent H2O2 signalling in their pathomechanisms.
Schallreuter
K U
KU
Clinical and Experimental Dermatology, Department of Biomedical Sciences, University of Bradford, BD7 1DP, Bradford, West Yorkshire, UK. K.Schallreuter@bradford.ac.uk
Kothari
S
S
Elwary
S
S
Rokos
H
H
Hasse
S
S
Panske
A
A
D002374:Catalase / Q000378:metabolism; D006801:Humans; D006836:Hydro-Lyases / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism; D009508:Nevus, Pigmented / Q000201:enzymology / Q000473:pathology*; D012878:Skin Neoplasms / Q000201:enzymology / Q000473:pathology*; D014820:Vitiligo / Q000201:enzymology / Q000473:pathology*; D044465:White People
D006861:Hydrogen Peroxide; D002374:Catalase; D006836:Hydro-Lyases; C076392:pterin-4a-carbinolamine dehydratase