ABSTRACT
Objective: To establish a system and method for screening plant extract against mitomycin C-induced genotoxic damage. Methods: Salmonella typhimurium TA1535/pSK1002 and acute toxicity experiment of mice were used, and the effects of the extracts from ten plants, Chrysanthemis Flos, Allii Bulbus, Zingiberis Rhizoma Recens, Ginkgo Folium, Ginseng Radix et Rhizoma, Vitis Viniferae Semen, Gemmae Camelliae Sinensis Folium, Ganoderma, Acanthopanacis Senticosi Radix et Rhizoma seu Caulis, and Sojae Semen, and the extract combinations on mitomycin C-induced genotoxic damage were observed by SOS/umu test. Results: Significantly protective effects of five extracts, including the extracts from Allii Bulbus, Vitis Vindferae Semen, Gemmae Camelliae Sinensis Folium, Acanthopanacis Senticosi Radix et Rhizoma seu Caulis, and Sojae Semen against mitomycin C-induced genotoxicity were observed. Acanthopanacis Senticosi Radix et Rhizoma seu Caulis extract (1.5 g/L) could inhibit the mitomycin C-induced genotoxicity (67.12%). Combinations of any two extracts showed higher antimutagenic capacity than any single one. Among all the combinations, Acanthopanacis Senticosi Radix et Rhizoma seu Caulis-Gemmae Camelliae Sinensis Folium and Acanthopanacis Senticosi Radix et Rhizoma seu Caulis-Vitis Viniferae Semen showed the highest activity, and the inhibition rate of the former against the mitomycin C-induced genotoxicity was 83.2%. In vivo tests showed that Acanthopanacis Senticosi Radix et Rhizoma seu Caulis- Gemmae Camelliae Sinensis Folium could significantly decrease the micronucleus rate and sperm abnormality rate of mice induced by mitomycin C and also increase the thymus indexes. Conclusion: Based on the results, it is clearly proved that the SOS/umu is not only a useful and convenient way to evaluate the antimutagenic ability of plant extracts, but also could be used as a kind of rapid screening model for cytoprotector with high throughput screening of candidate extracts or compounds.
ABSTRACT
OBJECT: The aim of this study is to determine whether exposure to chlorpromazine causes mutagenicity and genetic disorders. METHOD: Ames (Salmonella typhimurium) test and Rec assay (Bacillus subtilis) were used as indicators for DNA damage. Furthermore, the levels of umu operon expression by measuring the beta-galactosidase activity were monitered with the SOS umu test using S. typhimurium 1535 containing plasmid pSK1002. And the host-mediated assay was used to investigate the muta-genicity of chlorpromazine after the activation with in vivo metabolic systems. RESULTS: From the results, chlorpromazine did not affect DNA of S. typhimurium and B. subtilis strains and showed no mutagenicity at the all concentrations tested. These phenomena was also similar to that after metabolic activation of chlorpromazine in in vivo system. CONCLUSION: These results suggested that chlorpromazine did not show the mutagenicity and genotoxicity by four different methods used in this study.