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1 May 2005 Protective Effects of Cyanidin-3-O-β-glucopyranoside Against UVA-induced Oxidative Stress in Human Keratinocytes
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Ultraviolet-A (UVA) radiation causes significant oxidative stress because it leads to the generation of reactive oxygen species (ROS), leading to extensive cellular damage and eventual cell death either by apoptosis or necrosis. We evaluated the protective effects of cyanidin-3-O-β-glucopyranoside (C-3-G) against UVA-induced apoptosis and DNA fragmentation in a human keratinocyte cell line (HaCaT). Treatment of HaCaT cells with C-3-G before UVA irradiation inhibited the formation of apoptotic cells (61%) and DNA fragmentation (54%). We also investigated antioxidant properties of C-3-G in HaCaT cells against ROS formation at apoptotic doses of UVA; C-3-G inhibited hydrogen peroxide (H2O2) release (an indicator of cellular ROS formation) after UVA irradiation. Further confirmation of the potential of C-3-G to counteract UVA-induced ROS formation comes from our demonstration of its ability to enhance the resistance of HaCaT cells to the apoptotic effects of both H2O2 and the superoxide anion (O2·−), two ROS involved in UVA-oxidative stress. Furthermore, in terms of Trolox Equivalent Antioxidant Activity, C-3-G treatment led to a greater increase in antioxidant activity in the membrane-enriched fraction than in the cytosol (55% vs 19%). The protective effects against UVA-induced ROS formation can be attributed to the higher membrane levels of C-3-G incorporation. These encouraging in vitro results support further research into C-3-G (and other anthocyanins) as novel agents for skin photoprotection.

Andrea Tarozzi, Alessandra Marchesi, Silvana Hrelia, Cristina Angeloni, Vincenza Andrisano, Jessica Fiori, Giorgio Cantelli-Forti, and Patrizia Hrelia "Protective Effects of Cyanidin-3-O-β-glucopyranoside Against UVA-induced Oxidative Stress in Human Keratinocytes," Photochemistry and Photobiology 81(3), 623-629, (1 May 2005).
Received: 14 June 2004; Accepted: 1 January 2005; Published: 1 May 2005

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