Ascorbic acid 2-O-α-glucoside-induced redox modulation in human keratinocyte cell line, SCC: Mechanisms of photoprotective effect against ultraviolet light B

Abstract

We previously reported that the topical application of ascorbic acid 2- O-α-glucoside (AA-2G) suppressed the cutaneous inflammation by ultraviolet irradiation in human and guinea pigs (Miyai et al., Nishinihon J. Dermatol., 58, 439-3 (1996)). In this paper, the effect of AA-2G on the lethal damage induced by ultraviolet B (UVB) was studied using a human keratinocyte cell line, SCC, established from squamous cell carcinoma. The photoprotective effect of AA-2G on cytotoxicity of UVB in SCC cells was dose dependent (0.12- 1 mM) and more effective than that of ascorbic acid (AsA) at 1 nM. This protection was completely abolished in the presence of an α-glucosidase inhibitor, castanospermine, indicating that release of AsA from this derivative was essential for reduction of the actinic injury. AA-2G significantly suppressed cytotoxicities of hydrogen peroxide and superoxide anion produced by xanthine and xanthine oxidase. AA-2G exhibited a preventive effect against the cytotoxicity produced by tert-butylhydroperoxide, an inducer of lipid peroxidation, in the presence of α-tocopherol, but not in the absence of α-tocopherol. Cytotoxicity of UVB was also effectively reduced by the combination of AA-2G and α-tocopherol. In addition, AA-2G reduced UVB-promoted formation of lipid peroxide and accumulation of lipofuscin, which is known to be a complex of cellular proteins and metabolites of lipid peroxide. These data suggest that AA-2G prevents the acute inflammation induced by UVB irradiation partly through scavenging reactive oxygen species and potentiating the antioxidative activity of α- tocopherol.