Mokdad-Bzeouich Imen1, Fadwa Chaabane1, Mustapha Nadia1, Kilani-jaziri Soumaya1, Ghedira Kamel2, Chekir-Ghedira Leila3. 1. Laboratory of Cellular and Molecular Biology, Faculty of Dental Medicine, University of Monastir, Avicenne Street, 5000 Monastir, Tunisia; Unit of Bioactive and Natural Substances and Biotechnology UR12ES12, Faculty of Pharmacy of Monastir, University of Monastir, Avicenne Street, 5000 Monastir, Tunisia. 2. Unit of Bioactive and Natural Substances and Biotechnology UR12ES12, Faculty of Pharmacy of Monastir, University of Monastir, Avicenne Street, 5000 Monastir, Tunisia. 3. Laboratory of Cellular and Molecular Biology, Faculty of Dental Medicine, University of Monastir, Avicenne Street, 5000 Monastir, Tunisia; Unit of Bioactive and Natural Substances and Biotechnology UR12ES12, Faculty of Pharmacy of Monastir, University of Monastir, Avicenne Street, 5000 Monastir, Tunisia. Electronic address: leila.chekir@laposte.net.
Abstract
AIMS: The objective of this study was to examine the effect of eriodictyol on melanogenesis in cultured murine melanoma cells (B16-F10) and its antigenotoxic and antioxidant potentials on primary human keratinocyte (PHK) cells. MAIN METHODS: Anti-melanogenic effect was performed via the determination of melanin content and tyrosinase activity. Antigenotoxicity and antioxidant potentials were assessed by comet and cellular antioxidant assays, respectively. KEY FINDINGS: Eriodictyol reduced melanogenesis by inhibiting the tyrosinase activity of B16-F10 cells in a dose dependent manner. Its eventual genotoxicity was investigated by evaluating its capacity to induce DNA degradation of treated cell nuclei. As no genotoxicity was detected at the different tested concentrations, its ability to protect cell DNA against hydrogen peroxide (H2O2) oxidative effect in PHK cells was investigated using the "comet assay. It appears that 50 μM of eriodictyol solution suppressed H2O2 induced genotoxicity. In addition, this molecule revealed a significant cellular antioxidant capacity against reactive oxygen species formation in B16-F10 and PHK cells. SIGNIFICANCE: Thus, eriodictyol could be introduced as a natural skin depigmenting agent in skin care products.
AIMS: The objective of this study was to examine the effect of eriodictyol on melanogenesis in cultured murinemelanoma cells (B16-F10) and its antigenotoxic and antioxidant potentials on primary human keratinocyte (PHK) cells. MAIN METHODS: Anti-melanogenic effect was performed via the determination of melanin content and tyrosinase activity. Antigenotoxicity and antioxidant potentials were assessed by comet and cellular antioxidant assays, respectively. KEY FINDINGS:Eriodictyol reduced melanogenesis by inhibiting the tyrosinase activity of B16-F10 cells in a dose dependent manner. Its eventual genotoxicity was investigated by evaluating its capacity to induce DNA degradation of treated cell nuclei. As no genotoxicity was detected at the different tested concentrations, its ability to protect cell DNA against hydrogen peroxide (H2O2) oxidative effect in PHK cells was investigated using the "comet assay. It appears that 50 μM of eriodictyol solution suppressed H2O2 induced genotoxicity. In addition, this molecule revealed a significant cellular antioxidant capacity against reactive oxygen species formation in B16-F10 and PHK cells. SIGNIFICANCE: Thus, eriodictyol could be introduced as a natural skin depigmenting agent in skin care products.