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that are excreted to the skin surface and form sebum. The function of sebum is still a matter of investigation. It is only hypothesized that sebum may play a role in the protection of skin from dehydration, ultraviolet radiation (UVR), wrinkling, and infection ( 1, 2 ). The sebaceous lipid mixture is highly complex and consists of triacylglycerols (TAG), diacylglycerols (DAG), and free fatty acids (FFA), which together account for 50-60% of its composition. Sebum also contains 20-30% wax esters (WE), 10-16% squalene (SQ), and 2-4% cholesterol esters (CE) ( 1, 2 ). Initial analyses of the components of the sebaceous lipid mixture conducted by led to the identifi cation of several different types of acyl chains in esters with glycerol, cholesterol, and waxes. Fatty acids (FA) with an odd number of carbon atoms, branched side chains, and sites of unsaturation at unconventional positions were characterized. However, information on the intact lipids remained to be determined. A detailed characterization of the lipid repertoire in sebum in physiologic and diseased conditions is very limited due to the unavailability of methods for the comprehensive and simultaneous analysis of whole lipids. Prior investigations of the composition of sebum have been mostly concerned with acne, a multifactorial skin disorder that affects the pilosebaceous unit. Currently, only a few parameters are addressed when investigating alterations in sebum, such as SQ levels and the composition of FA obtained from the hydrolysis of TAG, DAG, WE, and CE. The methodology for the targeted analysis of SQ involves gas chromatography (GC) with Abstract Sebum is a complex lipid mixture that is synthesized in sebaceous glands and excreted on the skin surface. The purpose of this study was the comprehensive detection of the intact lipids that compose sebum. These lipids exist as a broad range of chemical structures and concentrations. Sebum was collected with SebuTape TM from the foreheads of healthy donors, and then separated by HPLC on a C8 stationary phase with sub 2 µm particle size. This HPLC method provided high resolution and excellent reproduc- Skin is a metabolically active tissue that contains sebaceous glands, which are specialized organelles equipped for the synthesis of a broad spectrum of lipid compounds

Vitiligo is characterized by the progressive disappearance of pigment cells from skin and hair follicle. Several in vitro and in vivo studies show evidence of an altered redox status, suggesting that loss of cellular redox equilibrium might be the pathogenic mechanism in vitiligo. However, despite the numerous data supporting a pathogenic role of oxidative stress, there is still no consensus explanation underlying the oxidative stress-driven disappear of melanocytes from the epidermis. In this study, in vitro characterization of melanocytes cultures from non-lesional vitiligo skin revealed at the cellular level aberrant function of signal transduction pathways common with neurodegenerative diseases including modification of lipid metabolism, hyperactivation of mitogen-activated protein kinase (MAPK) and cAMP response element-binding protein (CREB), constitutive p53-dependent stress signal transduction cascades, and enhanced sensibility to pro-apoptotic stimuli. Notably, these long-term effects of subcytotoxic oxidative stress are also biomarkers of pre-senescent cellular phenotype. Consistent with this, vitiligo cells showed a significant increase in p16 that did not correlate with the chronological age of the donor. Moreover, vitiligo melanocytes produced many biologically active proteins among the senescence-associated secretory phenotype (SAPS), such as interleukin-6 (IL-6), matrix metallo proteinase-3 (MMP3), cyclooxygenase-2 (Cox-2), insulin-like growth factor-binding protein-3 and 7 (IGFBP3, IGFBP7). Together, these data argue for a complicated pathophysiologic puzzle underlying melanocytes degeneration resembling, from the biological point of view, neurodegenerative diseases. Our results suggest new possible targets for intervention that in combination with current therapies could correct melanocytes intrinsic defects.

The data further support the involvement of lipid oxidation and particularly by-products of squalene oxidation in comedogenesis.