Enhancing Effect of Ultraviolet A on Ornithine Decarboxylase Induction and Dermatitis Evoked by 12-<i>o</i>-Tetradecanoylphorbol-13-Acetate and Its Inhibition by Curcumin in Mouse Skin

Abstract

Background: Previous studies have demonstrated appreciable tumor induction in mouse skin by daily irradiation with high-power long-wavelength ultraviolet A (UVA). Object: The aim of the present study was to examine the enhancing effects of UVA on changes in mouse skin mediated by the tumor promoter 12-o-tetradecanoylphorbol-13-acetate (TPA) by measurement of ornithine decarboxylase (ODC) activity and morphometric analysis. In addition, we examined the inhibitory effects of curcumin, a component of turmeric, on these changes. Method: ODC activity in the epidermis of CD-1 mice was determined by the method of Russell and Snyder. Epidermal and dermal thickness, and the number of dermal infiltrating inflammatory cells were quantified using a computer-assisted image analyzer. Results: A combination of topical TPA application and UVA irradiation produced a greater increment of ODC activity at 4 h than TPA alone (p < 0.05). Histopathologically, TPA plus UVA tended to increase the dermal infiltrating inflammatory cells in contrast to TPA alone. Pretreatment of mice with curcumin significantly abrogated the TPA-induced changes in ODC activity and the dermal infiltrating inflammatory cells as well as the TPA plus UVA-mediated enhancement of these changes. Conclusion: Our data indicate that UVA irradiation (18.72 J/cm²) significantly enhances ODC induction at an early stage (4–6 h) after topical application of TPA, and aggravates the dermatitis elicited by TPA. Pretreatment with curcumin significantly inhibits these enhancing effects.

Protection of normal human reconstructed epidermis from UV by catalase overexpression

“…54 Both keratinocyte hypertrophy and the increase in ODC induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) (enhancer of H 2 0 2 formation) or TPA þ UVA were prevented by the ROS inhibitor 1 0 -acetoxychavicol acetate 55 or by a vegetal antioxidant. 56 It is well known that UVA does not interact directly with DNA, but instead appears to contribute to DNA damage through ROS, resulting in oxidative DNA modifications, including the formation of 8-oxodG, protein-DNA crosslinking, base loss and strand breaks. 1,46 Decrease in UVAinduced DNA oxidation (8-oxodG) in RE overexpressing CAT is consistent with this notion.…”

Chemoprevention of photocarcinogenesis by selected dietary botanicals

“…Curcumin protects cultured human cells from radiationinduced DNA damage and this effect may be due to its strong antioxidant properties. 63 Ishizaki et al 64 observed that topical application of curcumin significantly inhibited TPA-and UVAinduced ornithine decarboxylase activity in mouse epidermis. Oguro and Yoshida 65 have also confirmed this investigation and reported that topical application of curcumin inhibits TPA-and UVA-induced gene expression of metalloprotein in the mouse skin and postulate that these chemopreventive effects may be due to its role as an ROS scavenger.…”

Chemoprevention of Skin Cancer with Dietary Phytochemicals

“…Topical administration of the curcumin has been represented to enhance glutathione contents and glutathione-S-transferase (GST) activity, and suppresses lipid peroxidation and COX-2 activation in mouse skin and human IGR-39 melanoma cells (Iersel et al, 1996). Also, curcumin has been represented to attenuate the induction of ornithine decarboxylase (ODC) in mouse skin (Ishizaki et al, 1996) and to induce p53-associated apoptotic cell death through the blocking the NF-κB pathway and inhibiting the apoptotic inhibitor XIAP (X-linked inhibitor of apoptosis protein) in human basal carcinoma cells (Jee et al, 1998). These researches suggest that curcumin could be beneficial chemopreventive agent against the skin cancer (F'guyer et al, 2003).…”