UV-induced skin carcinogenesis

UV-induced skin carcinogenesis by azthioprine (216), photochemical interaction between triamterene and hydrochlorthiazide (217) photochemistry of diclofenac (218), kinetic treatment of photochemical reactions (219) and a direct electron paramagnetic resonance (EPR) and spin-trapping study of light-induced free radicals from 6-mercaptopurine and its oxidation products (220). 

Kelly GE, Meikle WD, Moore DE. Promotion of UV-induced skin carcinogenesis by azathioprine role of photochemical sensitization. Photochem Photobiol 1989 49 59-65. Moore DE, MaUesch JL. Photochemical interaction between triamterene and hydro-chlorthiazide. Int J Pharm 1991 76 187-190. 

Reasons to Suspect Drug May Enhance UV-induced Skin Carcinogenesis... 

Table V. Inhibitory Effect of DBM and PABA on UV-induced Skin Carcinogenesis in SKH-1 Mice Previously Treated with DMBA...

The last experiment was repeated in part using hr/hr Oslo strain mice and extended by the use of SEN mice. The data were mainly presented as summary statistics. In contrast to the earlier results, the gel without benzoyl peroxide did not enhance DMBA carcinogenesis in hr/hr mice and Panoxyl did not enhance DMBA carcinogenesis in SEN mice. Groups of 32 hr/hr mice were also treated with ultraviolet radiation (UV) from new Phillips HP 3114 sunlamps, either alone twice a week or 5-30 min before treatment with Panoxyl or the gel without benzoyl peroxide. The numbers of mice with skin carcinomas (and the total numbers of skin tumours in each group of mice) were UV alone, 26/32 (103 papillomas, 45 carcinomas) UV + Panoxyl, 22/32 (94 papillomas, 30 carcinomas) UV + gel, 23/32 (126 papillomas, 29 carcinomas). Thus, neither Panoxyl nor the gel without benzoyl peroxide had any significant effect upon the multiplicity of UV-induced skin tumours (Iversen, 1988). 

Overvad K, Thorling E, Bjerring PEP. 1985. Selenium inhibits UV-light-induced skin carcinogenesis in hairless mice. Cancer Lett 27 163-170. 

In the second experiment, mice were irradiated with the highest dose from the dose-response experiment. Concentrations of lipid hydroperoxides and lipophilic antioxidants were measured simultaneously on single skin samples from irradiated and non-irradiated sides of each mouse. The lipid hydroperoxide assay directly measured lipid peroxidation and thus was superior to the TBARS assay, which is indirect. Lipid-peroxyl radicals have been linked to chemically induced cutaneous carcinogenesis [31] as well as to UV-light-induced cutaneous carcinogenesis [32],... 

UV is known to induce nonmelanoma skin cancer. Ethanol and aloe emodin alone do not induce skin tumors in the absence of UV. When an ethanol solution of aloe emodin was painted onto the skin of mice in conjunction with UVB exposure, the mice developed melanin-containing skin tumors. The mechanism for the observed carcinogenesis induction by the mixture is unknown, 91... 

Two stage mouse skin carcinogenesis induced with DMBA and promoted with UV (B-region) irradiation Oral administration of the extracts exhibited inhibitory effect. 

Some of the recently isolated triterpenes possessed antitumor and cancer chemo-preventive activities. The chemopreventive activity was displayed in a mouse skin carcinogenesis assay, a UV-induced photocarcinogenesis assay in mice, and a TPA-induced Epstein-Barr vims early antigen activation assay in vitro. The antitumor activity was demonstrated in vitro in a panel of 39 human cancer cell lines. ... 

Protective Effect of Dibenzoylmethane on Chemically- and UV Light-Induced Skin, Inflammation, Sunburn Lesions, and Skin Carcinogenesis in Mice... 

The protective effect of DBM and PABA on UV-induced complete skin carcinogenesis also was examined and the results were shown in Table VI. Irradiation of 30 mJ/cm UV to female SKH-1 mice twice a week for 34 weeks resulted in formation of 6 skin tumors per mouse and 90% of mice had skin tumors. Topical application 10 pmol DBM or 10 pmol PABA at 10 min prior each UV irradiation twice a week for 34 weeks inhibited the number of skin tumors per mouse by 95.9% and 88.4%, respectively. The percentage of mice with skin tumors was inhibited by 80% and 48%, respectively (Table VI). The results suggest that DBM had a better protective action on UV-induced complete skin carcinogenesis imder these conditions. 

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