Ultraviolet (UV) has been shown to be an inducer of apoptosis. We have reported that UVB was a causative factor of apoptosis in the mouse keratinocytes in vivo and in vitro, and that sunburn cell (SBC) appearing in the epidermis after UVB irradiation was apoptotic cell. On the other hand, some antioxidants including superoxide dismutase and catalase, are known to inhibit UVB-induced SBC formation. Recently we found that β-thujaplicin, hinokitiol (4-isopropyl tropolone), had direct activity as an antioxidant. In this study, we examined the effect of β-thujaplicin on UVB-induced apoptosis in keratinocytes. First, mouse ear skin treated with β-thujaplicin was irradiated with UVB dose of 150 mJ/cm 2 . Twenty four hours after irradiation, the skin was biopsied and stained with H&E for SBC counting. The numbers of SBCs were significantly reduced in β-thujaplicin-treated mice. Secondly, cultured mouse keratinocytes (PAM212) incubated with β-thujaplicin were irradiated with UVB dose of 50mJ/cm 2 . Twenty four hours after irradiation, DNA was isolated from these cells and was processed to observe DNA ladder characteristic to apoptosis. The ladder formation was significantly inhibited in β-thujaplicin-treated cells. In addition, in PAM212 cells, we demonstrated that β-thujaplicin induced mRNA of metallothionein, which is known to have scavenging activity for reactive oxygen species through its abundant cystein residues. Our data suggest that these inhibitory effects on UVB-induced apoptosis are due to direct and indirect antioxidant activities of β-thujaplicin.