• Applied Biological Chemistry
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• v.39 no.6
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• pp.424-429
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• 1996

Inhibitory mechanism of colored rice bran against cellular genotoxicity induced by chemical mutagen was studied using organic solvent extracts from a colored rice cultivar termed as Suwon415, and the mutagen, mitomycin C. Inhibitory effects of 70% ethanol extact and chloroform fraction from rice bran of Suwon415 were higher than those from Chuchung used as control. However, antioxidative activities of each fraction from Suwon415 were slightly lower than those from Chuchung, suggesting the involvement of a different inhibitory mechanism not related to antioxidation pathway. Using E. coli as the indicator cell, inhibitory mechanism of rice bran extract from colored rice against mutagenicity induced by mitomycin C was investigated to reveal the possibility that it acts in a desmutagenic manner. Further investigation to quantify the free mitomycin C in reaction mixture following incubation with rice bran extract demonstrated that rice bran extract might inhibit the cellular genotoxicity of mitomycin C by direct adsorption of the mutagen.

• The Korean Journal of Food And Nutrition
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• v.9 no.3
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• pp.294-298
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• 1996

By the 505 chromotest which utilized Escherichia bolt PQ 37, Korean medicinal plants had been screened to Investigate the antimutagenic effect to aflatoxin B1(AFBl). Ikmocho(IMC, Leonurus sibiricus L.) was extracted with hot water. The extract was not found to be mutagenic in the Salmonella mutation test with or without metabolic activation, and the extract was showed to possess the antimutagenic properties towards AFB1-induced metation. The mutagenicity of AFB1 was inhibited by methanol soluble fracstion (IMC-MS) in dose-dependent. However, water-soluble fraction exhibited comutagenic activity. The greatest inhibitory effect of IMC-MS on AFB1 mutagenicity occurred when IMC-MS was first incubated, AFB1 followed by a second incubation with the cells and 59 mixture. Also lower inhibition was occurred when S9 mixtures were first incubated, with IMC-MS followed by a second incubation with AFBI. The results of the sequential incubation study support the probability that one mechanism of inhibition could involve the formation of chemical complex between IMC-MS and AFB1 rather than deactivation of S9 enzyme.