Mitochondrial impairment in peripheral blood mononuclear cells during the active phase of vitiligo

Several hypotheses have been made about the pathogenesis of vitiligo, and s ome of them have considered a systemic involvement in the course of the dis ease. Evidence has been presented on the role of oxidative stress as the in itial event in melanocyte degeneration. In accordance with this view, we de termined the levels of some antioxidants, i.e., superoxide dismutase, catal ase, reduced glutathione, and vitamin E, in erythrocytes and/or peripheral blood mononuclear cells from patients with active or stable vitiligo and fr om a control group of healthy subjects. In erythrocytes the parameters eval uated were not significantly different. On the contrary, in peripheral bloo d mononuclear cells, superoxide dismutase activity was increased in both gr oups of patients, whereas catalase activity, reduced glutathione and vitami n E levels were decreased exclusively in subjects with active disease. The imbalance of antioxidants was associated with hyperproduction of reactive o xygen species due to a mitochondrial impairment as cyclosporin A, an inhibi tor of the permeability transition pores opening, significantly reduced the reactive oxygen species production. Moreover an alteration of the mitochon drial transmembrane potential and a higher percentage of apoptotic cells we re observed in active vitiligo patients. Based on these results, we suggest that, in vitiligo, mitochondria might be the target of different stimuli, such as reactive oxygen species generation, cytokines production, catechola mine release, alteration of Ca2+ metabolism, all of which capable of induci ng melanocyte degeneration.