BACKGROUND: The objective of the present study was to determine if modulation of GSH-dependent antioxidant protective system by Brassica oleraceae var capitata might inhibit the molecular mechanism of skin tumor promotion. MATERIALS AND METHODS: In a two stages skin carcinogenesis model, the protocol used included a single topical application of 200 nmol of the initiator 7,12-dimethyl-benz(a) anthracene (DMBA) to the backs of mice, followed 1 week later by promotion with 10 nmol of 12-O-tetradecanoyl-phorbol-13 acetate (TPA) twice weekly for 30 weeks. In addition to this regimen, 0.1 g/L brassica extract was added water week prior to the initiating dose of DMBA in the treatment group. Tissue glutathione (GSH) contents and levels of lipid peroxidation products (measured as thiobarbituric-acid (TBA)-reactive substances) were quantitated in the skin tumors generated by the initiation-promotion protocol. RESULTS: It was observed that the tumor incidence and tumor multiplicity in the treatment group was highly significantly low compared to the first group of mice (p < 0.001 and p < 0.001, respectively). In the treatment group, GSH content in the papillomas was higher than in the non-involved skin surrounding the papillomas. CONCLUSIONS: We suggest that the anticarcinogenicity of Brassica may be linked to its ability to facilitate or enhance the activity of the natural GSH-dependent antioxidant protective system of the epidermal cells during the later stages of skin tumor promotion.
BACKGROUND: The objective of the present study was to determine if modulation of GSH-dependent antioxidant protective system by Brassica oleraceae var capitata might inhibit the molecular mechanism of skin tumor promotion. MATERIALS AND METHODS: In a two stages skin carcinogenesis model, the protocol used included a single topical application of 200 nmol of the initiator 7,12-dimethyl-benz(a) anthracene (DMBA) to the backs of mice, followed 1 week later by promotion with 10 nmol of 12-O-tetradecanoyl-phorbol-13 acetate (TPA) twice weekly for 30 weeks. In addition to this regimen, 0.1 g/L brassica extract was added water week prior to the initiating dose of DMBA in the treatment group. Tissue glutathione (GSH) contents and levels of lipid peroxidation products (measured as thiobarbituric-acid (TBA)-reactive substances) were quantitated in the skin tumors generated by the initiation-promotion protocol. RESULTS: It was observed that the tumor incidence and tumor multiplicity in the treatment group was highly significantly low compared to the first group of mice (p < 0.001 and p < 0.001, respectively). In the treatment group, GSH content in the papillomas was higher than in the non-involved skin surrounding the papillomas. CONCLUSIONS: We suggest that the anticarcinogenicity of Brassica may be linked to its ability to facilitate or enhance the activity of the natural GSH-dependent antioxidant protective system of the epidermal cells during the later stages of skin tumor promotion.