ANTICANCER RESEARCH, cilt.20, ss.219-224, 2000 (SCI-Expanded)
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 I 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.