The effects of the oral supplementation of L-Cystine associated with reduced L-Glutathione-GSH on human skin pigmentation: a randomized, double-blinded, benchmark- and placebo-controlled clinical trial.

BACKGROUND: Glutathione has become a potential skin-lightening ingredient after the discovery of its anti-melanogenic properties. Various mechanisms of action have been considered to explain this property, one of them being the skewing of the melanin synthesis pathway toward the production of lighter pheomelanin instead of darker eumelanin, consequently producing a lightening effect. AIMS: To evaluate the skin lightening and anti-dark spot effects of oral supplementation with L-Cystine associated with L-Glutathione as compared to placebo and benchmark. METHODS: Effects of this L-Cystine-L-Glutathione oral combination were investigated in a 12-week randomized, double-blind, parallel-group, benchmark- and placebo-controlled trial involving 124 Asian female subjects. Women were randomly allocated into 4 equal groups (500 mg L-Cystine and 250 mg L-Glutathione, 250 mg reduced L-Glutathione, 500 mg L-Cystine, or a placebo, daily). Skin color was measured at baseline, after 6 and 12 weeks by spectrophotometry. Size and color of facial dark spots were determined from digital photographs. RESULTS: A significant skin lightening was observed after 12 weeks of oral supplementation with L-Cystine associated with L-Glutathione. This combination also induced a significant reduction in the size of facial dark spots after 6 and 12 weeks. It is noteworthy that the observed effects were not only significantly better than those obtained with placebo, but also with L-Cystine alone or L-Glutathione alone. CONCLUSION: The daily oral administration of 500 mg L-Cystine and 250 mg L-Glutathione during 12 weeks was a safe treatment to effectively lighten the skin and reduce the size of facial dark spots of Asian women.

Age-dependent response of energy metabolism of human skin to UVA exposure: an in vivo study by 31P nuclear magnetic resonance spectroscopy.

PURPOSE: The aim of our study was to evaluate the in vivo energy metabolism of human skin as a function of age, in conditions of rest and after a mild stress caused by a suberythemal UVA irradiation. METHODS: The kinetics of UVA-induced modifications in high-energy phosphorylated metabolites of young and old skins were non-invasively monitored over a period of 24 h using 31P nuclear magnetic resonance spectroscopy. In vivo 31P spectra were obtained on the ventral aspect of the wrist, using a NMR Imaging Spectrometer equipped with a double-tuned surface coil. Concentrations of phosphocreatine, inorganic phospate, adenosine tri-phosphate, phosphomono and phosphodiesters were calculated from the spectra and results were expressed as relative concentrations. A total of 20 subjects were enrolled in this study (n = 10 for the age group below 25 years and n = 10 for the age group above 55 years). A second experiment was then performed on 10 old subjects (mean age 60) who were treated on one wrist, twice a day for one month prior to UVA irradiation, with a product that contained active ingredients to restore barrier function and modulate the inflammatory response, the other wrist being an untreated control. RESULTS: Baseline levels of phosphorylated metabolites were similar in young and old skins. A suberythemal dose of UVA (6 J.cm-2) led to a significant decrease in the PCr/Pi ratio (index of energy status) and a significant increase in the PME/PDE ratio (index of cellular turnover rate of lipid-related metabolites) within 1 h. The observed variations were transient and the recovery was complete at T + 24 h post-UVA, although recovery was significantly slower in the older group. The disturbances were significantly reduced after treatment of the older skin with a formula that restored barrier function of the stratum corneum and modulated the inflammatory response. CONCLUSION: (i) baseline levels of energy metabolites in skin do not seem to vary with age; (ii) low dose UVA irradiation induces a rapid response in the energy metabolism of the skin; (iii) the kinetics of the response and recovery after an aggression by UVA suggest that older skin has significantly less energy rebound after a stress situation than younger skin; (iv) the energy reserve in older skin can be protected efficiently against UVA-induced stress by restoring barrier function and modulating the inflammatory response.