Date Seed Oil Inhibits Hydrogen Peroxide-Induced Oxidative Stress in Normal Human Epidermal Melanocytes

• Published in: Connective tissue research Vol. 50; no. 5; pp. 330 - 335
• Main Authors: Dammak, Ines, Boudaya, Sonia, Abdallah, Fatma Ben, Hamida, Turki, Attia, Hamadi
• Format: Journal Article
• Language: English
• Published: England Informa UK Ltd 2009; Taylor & Francis
• Subjects: Antioxidants - pharmacology; Antioxidants - therapeutic use; Catalase - drug effects; Catalase - metabolism; Cell Culture; Cell Survival - drug effects; Cell Survival - physiology; Cells, Cultured; Date Seed Oil; Dose-Response Relationship, Drug; Epidermis - cytology; Epidermis - drug effects; Epidermis - metabolism; Free Radical Scavengers - pharmacology; Free Radical Scavengers - therapeutic use; Glutathione Peroxidase - drug effects; Glutathione Peroxidase - metabolism; Humans; Hydrogen Peroxide - antagonists & inhibitors; Hydrogen Peroxide - toxicity; Lipid Peroxidation - drug effects; Lipid Peroxidation - physiology; Melanocytes - drug effects; Melanocytes - metabolism; Normal Human Epidermal Melanocytes; Oxidants - antagonists & inhibitors; Oxidants - toxicity; Oxidative Stress; Oxidative Stress - drug effects; Oxidative Stress - physiology; Plant Extracts - pharmacology; Plant Extracts - therapeutic use; Plant Oils - pharmacology; Plant Oils - therapeutic use; Seeds - chemistry; Superoxide Dismutase - drug effects; Superoxide Dismutase - metabolism; Wound Healing - drug effects; Wound Healing - physiology
• ISSN: 0300-8207; 1607-8438
• DOI: 10.1080/03008200902836073

The administration of antioxidants has been shown to enhance repair and healing processes in cutaneous tissue. Date seed oil (DSO) extract, which might be a potential source of natural antioxidants such as phenols and tocopherols, has been reported to be beneficial in the reduction of chemically induced oxidative stress in normal human skin. In this study, we investigated the protective effects of DSO against hydrogen peroxide (H2O2)-induced oxidative stress in terms of lipid peroxidation, depletion of such endogenous antioxidant defense enzymes as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) using normal human epidermal melanocytes (NHEM). The results showed that DSO, endowed with a radical scavenging ability, decreased oxidative injury by inhibition of damage caused by H2O2. Treatment of NHEM with DSO inhibited H2O2-induced lipid peroxidation. In addition, the extract inhibited H2O2-induced depletion of antioxidant defense components, such as SOD, CAT, and GPx. Our findings demonstrate that DSO is an efficient extract able to prevent melanocytes oxidative damage induced by H2O2 exposure. Thus it may be a potential promising candidate, as a chemopreventive agent, in the development of melanocyte-related pathologies like vitiligo and melanoma.