We have previously reported that patients with active vitiligo (AVP) h
ave elevated urinary levels of catecholamine metabolites, such as homo
vanillic and vanilmandelic acids, irrespective of the form of the dise
ase (acrofacial, segmental, generalized). We have suggested that abnor
mal release of catecholamines from autonomic nerve endings might play
an etiological role in the onset and development of vitiligo through a
n overproduction of toxic (oxy)radicals in the microenvironment of mel
anocytes in the affected areas. In the present study we have investiga
ted whether this suggested increase in radicals might be associated wi
th an oxidative stress in the blood of AVP. We have analyzed by gas-ch
romatography mass-spectrometry, by high pressure liquid chromatography
, by spectophotometry plasma levels of vitamin E (Vit E), lipoperoxide
s (LIP), and polyunsaturated fatty acids of phospholipids (PL-FA), ery
throcyte reduced glutathione (GSH), glutathione peroxidase (GSH-Px), a
nd superoxide dismutase (SOD) activities in 62 patients affected with
different forms of active vitiligo (acrofacial, segmental, generalized
) and in 60 age-matched controls. Our results show that blood levels o
f Vit E, SOD, GSH, GSH-Px activity, LIP and PL-FA in AVP were not sign
ificantly different from those of healthy age matched controls, indica
ting that melanocyte damage in vitiligo is not linked with a generaliz
ed oxidative stress.