1. ¹Laboratory of Cutaneous Physiopathology, IRCCS, Rome, Italy
2. ²Unity of Phototherapy, IRCCS, Rome, Italy
3. ³Department of Clinical Dermatology of San Gallicano Dermatological Institute, IRCCS, Rome, Italy
4. ⁴Department of Biological Sciences, Modena e Reggio Emilia University, Modena, Italy
5. ⁵Department of Biology, Tor Vergata Unversity, Rome, Italy

Correspondence: Dr Mauro Picardo, Laboratory of Cutaneous Physiopathology, San Gallicano Dermatological Institute, IRCCS, Via San Gallicano 25/a, Rome 00153, Italy. E-mail: picardo@ifo.it; citolab@ifo.it

Received 27 July 2006; Revised 29 September 2006; Accepted 18 October 2006; Published online 18 January 2007.

Abstract

The occurrence of oxidative stress has been proposed as a pathogenetic mechanism for melanocyte degeneration in vitiligo. In order to evaluate this possible correlation we focused on the lipid component of cell membranes. We observed in vitiligo melanocytes, through FACS methods, an increased median fluorescence intensity of rhodamine 123 and C11-BODIPY581/591 indicating a spontaneous higher production of reactive oxygen species (ROS) and membrane lipoperoxidation, associated with an altered pattern of cardiolipin (CL) distribution, defined on the basis of the fluorescence pattern after staining with 10-nonyl acridine orange. We confirmed membrane peroxidation by confocal and contrast-phase microscopes and demonstrated impaired activity of the mitochondrial electron transport chain (ETC) complex I. Finally, we observed increased apoptotic events following exposure to the pro-oxidant cumene hydroperoxide by Annexin V/propidium iodide fluorescence. We hypothesize that in vitiligo melanocytes lipid instability, with a defect in the synthesis or recycling of CL, induces ETC impairment and ROS production. In basal conditions melanocytes maintain the redox balance whereas following chemical or physical stress ROS-mediated membrane peroxidation is increased with a possible further CL oxidation, leading to cell death or detachment.