UV irradiation-induced zinc dissociation from commercial zinc oxide sunscreen and its action in human epidermal keratinocytes

Abstract

Zinc oxide (ZnO) is an active ingredient in sunscreen owing to its properties of broadly filtering the ultraviolet (UV) light spectrum and it is used to protect against the carcinogenic and photodamaging effects of solar radiation on the skin. This study investigated the dissociation of zinc (Zn2+) from ZnO in commercial sunscreens under ultraviolet type B light (UVB) irradiation and assessed the cytotoxicity of Zn2+ accumulation in human epidermal keratinocytes (HEK). Using Zn2+ fluorescent microscopy, we observed a significant increase in Zn2+ when ZnO sunscreens were irradiated by UVB light. The amount of Zn2+ increase was dependent on both the irradiation intensity as well as on the ZnO concentration. A reduction in cell viability as a function of ZnO concentration was observed with cytotoxic assays. In a real-time cytotoxicity assay using propidium iodide, the treatment of UVB-irradiated ZnO sunscreen caused a late- or delayed-type cytotoxicity in HEK. The addition of a Zn2+ chelator provided a protective effect against cellular death in all assays. Furthermore, Zn2+ was found to induce the production of reactive oxygen species (ROS) in HEK. Our data suggest that UVB irradiation produces an increase in Zn2+ dissociation in ZnO sunscreen and, consequently, the accumulation of free or labile Zn2+ from sunscreen causes cytotoxicity and oxidative stress. © 2010 Wiley Periodicals, Inc.