Superoxide dismutases (SODs) are believed to play a crucial role in protecting cells against oxygen toxicity. There are three forms of SOD: cytosolic Cu-Zn SOD, mitochondrial Mn SOD, and extracellular SOD (EC SOD). Extracellular SOD is primarily a tissue enzyme, but the role of EC SOD in skin is unclear. Therefore, this study investigated the distribution of EC SOD in the skin using immunohistochemistry and examining the patterns of EC SOD gene expression following ultraviolet (UV) irradiation in comparison with those of Cu-Zn SOD and Mn SOD in mouse dorsal skin using Northern blot analysis. Immunohistochemical analysis showed that EC SOD was abundantly located in the epidermis as well as in the dermis, but the gene expression of EC SOD mRNA was more abundant in the dermis than in the epidermis. The gene expression levels of all three types of SODs after UV irradiation were induced differently according to the type and UV irradiation dose. The EC SOD mRNA expression level was increased relatively later than that of Cu-Zn SOD and Mn SOD. The EC SOD mRNA level was significantly higher at 6 h and 48 h after UVA irradiation and psoralen plus ultraviolet-A treatment, respectively. Ultraviolet-B irradiation increased the EC SOD mRNA expression level, with maximum at 48 h. These suggest that EC SOD participates in the majority of antioxidant systems in the skin, and it may have different defensive roles from Cu-Zn SOD and Mn SOD against UV-induced injury of the skin.
Among Korean patients with psoriasis vulgaris, maintenance treatment with calcipotriol monohydrate/betamethasone dipropionate using a continuous daily regimen or an 'as needed' daily regimen provided similar efficacy, whereas a twice-weekly regimen was significantly less efficacious than either of these regimens.
Inappropriate apoptosis results in the epidermal hyperplasia as in psoriasis and UVB irradiation has been successfully used to treat this kind of skin disorders. Previously, we reported that the novel phytosphingosine derivative, tetraacetyl phytosphingosine (TAPS) induced apoptosis in HaCaT cells. This study examined the effect of UVB irradiation and/or TAPS on the induction of apoptosis in HaCaT. 10 mJ/cm2 of UVB irradiation or 10 microM of TAPS alone exhibited weak cytotoxicity but co-treatment of UVB and TAPS synergistically enhanced the cytotoxicity and apoptosis in HaCaT. The cells treated with UVB and TAPS showed much higher levels of cleaved caspase-3, -8, -9 and Bax than with UVB or TAPS alone, whereas Bcl-2 level was decreased by co-administration of UVB and TAPS. In hairless mice, co-treatment of UVB and TAPS synergistically increased apoptosis, as shown in the HaCaT co-treated with UVB and TAPS. Furthermore, UVB irradiation caused an increase of apoptotic cells in the epidermis and the TAPS-treated mice showed an increase of apoptotic cells in the dermis as well as in the epidermis. These results suggest that the TAPS co-treatment synergistically increases the level of UVB-induced apoptosis via caspase activation by regulating the level of pro-apoptotic Bax and anti-apoptotic Bcl-2.
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