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. © 2007 The Society for Investigative Dermatology.

Dell'Anna, M.L., Ottaviani, M., Albanesi, V., Vidolin, A.P., Leone, G., Ferraro, C., et al. (2007). Membrane lipid alterations as a possible basis for melanocyte degeneration in vitiligo. JOURNAL OF INVESTIGATIVE DERMATOLOGY, 127(5), 1226-1233 [10.1038/sj.jid.5700700].

Membrane lipid alterations as a possible basis for melanocyte degeneration in vitiligo

ROSSI, LUISA;
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. © 2007 The Society for Investigative Dermatology.
Pubblicato
Rilevanza internazionale
Articolo
Esperti anonimi
Settore BIO/10
eng
Con Impact Factor ISI
acridine orange; carbon 11; cardiolipin; cumene hydroperoxide; lipocortin 5; membrane lipid; propidium iodide; reactive oxygen metabolite; rhodamine 123; apoptosis; article; cell death; cell degeneration; cell membrane; confocal laser microscopy; controlled study; correlation analysis; electron transport; fluorescence activated cell sorting; human; human cell; lipid peroxidation; melanocyte; physical stress; priority journal; synthesis; vitiligo; Apoptosis; Benzene Derivatives; Biopsy; Cardiolipins; Cell Survival; Electron Transport Complex I; Humans; Lipid Peroxidation; Melanocytes; Membrane Lipids; Oxidants; Oxidative Stress; Reactive Oxygen Species; Skin; Vitiligo
Dell'Anna, M.L., Ottaviani, M., Albanesi, V., Vidolin, A.P., Leone, G., Ferraro, C., et al. (2007). Membrane lipid alterations as a possible basis for melanocyte degeneration in vitiligo. JOURNAL OF INVESTIGATIVE DERMATOLOGY, 127(5), 1226-1233 [10.1038/sj.jid.5700700].
Dell'Anna, M; Ottaviani, M; Albanesi, V; Vidolin, A; Leone, G; Ferraro, C; Cossarizza, A; Rossi, L; Picardo, M
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2108/35086
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