• Journal of the Korean Society of Food Science and Nutrition
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• v.27 no.4
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• pp.745-750
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• 1998

The antimutagenic and antigenotoxic effects of ethanol, methanol, water and non-heating ethanol extract of Ligularia fischeri were investigated using Ames test and micronucleus test. Four solvent extracts by themseleves did not induce mutagenesis. The four extract of 200㎍/plate showed approximately 84.7%, 77.1%, 72.5% and 71% inhibitory effect on the mutagenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine(MNNG) and 67.9%, 66.8%, 64.6% and 56% inhibition on the mutagenesis by 4-nitroquinoline-1-oxide(4NQO) against TA100 strain, whereas 70.2%, 60.9%, 61.9% and 52.8% inhibitions were observed on the mutagenesis induced by 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indol(Trp-P-1) in the presence of 200㎍/plate. TA100 strain was more sensitive than TA98 strain by four kinds of extracts on antimutagenesis. The effects of Ligularia fischeri extracts on the frequencies of micronucleated poly chromatic erythrocytes(MNPECs) induced by MNNG were investigated in the bone marrow. Ten, 20, 40 and 80mg g/kg of each extract were administered to animals immediately after injection of MNNG and the exposure time was 36 hours. Inhibitory effects of Ligularia fischeri ethanol extracts were 12%, 35.3%, 58.8%, and 57%, in the presence of 20, 40, 60 and 80mg/kg, respectively whereas methanol extracts showed 15.5%, 32.7%, 50.8%, and 57.9% inhibitory effects, respectively. Both extracts showed enhanced antimutagenic and antigenotoxic effects. These results showed a good correlation between antimutagenic effects in in vitro and in in vitro assay.

• Journal of the Korean Society of Food Science and Nutrition
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• v.21 no.1
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• pp.70-75
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• 1992

This study was carried out to investigate the characteristics of a mutant, Pseudomonas maltophilia H-8M selected with the treatment of Pseudomonas maltophilia H-8 by N-methyl-N-nitro-N-nitrosoguanidine(MNNG). This mutant showed highest ability of cadmium accumulation. The growth rate of Pseudomonas maltophilia H-8M showed about 80% in 1000ppm Cd containing medium when compare with control for 36h at $30^{\circ}C$. Pseudomonas maltophilia H-8M not inhibited on the growth in addition of various heavy metal such as $Hg^{2+}$, $Zn^{2+}$, $Pb^{2+}$, $Cu^{2+}$, $Cr^{2+}$ and $Co^{2+}$, but inhibited in $Sn^{2+}$ containing medium, respectively. Pseudomonas maltophilia H-8M was accumulated the highest cadmium level of 62.3% on whole cell in the medium containing 50 ppm and 80% of accumulated cadmium was distributed in the cell wall.

• Korean Journal of Food Science and Technology
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• v.23 no.3
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• pp.370-374
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• 1991

The inhibitory effects of garlic on the mutagenicity in Salmonella assay system and on the growth of HT-29 human colon carcinoma cells were studied. Methanol extract of garlic inhibited the mutagenicities induced by aflatoxin $B_1(AFB_1)$and N-methyl-N'-nitro-N-nitrosoguanidine(MNNG) in Salmonella typhimurium TA100. The inhibition rate increased significantly when the concentration of the methanol extract from garlic increased in both strains of Salmonella typhimurium TA98 and TA100. The chloroform fraction from the methanol extract exhibited strong antimutagenicity against $AFB_1$. The chloroform fraction also inhibited greatly the growth of human HT-29 colon carcinoma cells in fetal bovine serum concentrations of 1% and 5%.

• Preventive Nutrition and Food Science
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• v.3 no.2
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• pp.169-174
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• 1998

Antimutagenic and anticarcinogenic effects of alginic acids extracted from sea mustard(SM) and sporophyII of sea mustard(SSM) were studied by Salmonella typhimurium assay system and cytotoxicity and transformation tests using C3H/10T1/2 cells, respectively. alginic acid-SM andalginic acid-SSM showed antimutagenic effects on aflatoxin B1(AFB1)and N-methyl-N'-nitro-N-nitrosoguanidine(MNNG) in Salmonella typhimurium TA100 strain. The antimutagenic effect showed concentration dependent manner. At the 2.5mg/plate concentration , alginic acid-SSM exhibited 92% antimutagenicity against AFB1 ,while alginic acid-SM revealed 54% antimutagenictity ,s howing effectiveness of the alginic acid-SSM for the antimutagenicity. Alginic acidSSm also significantly decreased the cytotoxicity induced by 3-methylcholanthrene(MCA) and MNNG in C3H/10T1/2 cells (p<0.05). The type II and type IIItransformation foci formation by MCA and MNNG were also decreased when the alginic acid-SSM was treated, indicating that the alginic acid -SSM reduces the carcinogenesis induced by these carcinogens. The MCA-treated culture produced 10.5foci of type II +III in C3H/10T1/2 cells, however, MCA + 0.2mg/ml alginic acid-SSM treated culture formed only 1.8 foci of the types II + III in C3H/10T1/2 cells, however , MCA+0.2mg/ml alginic acid -SSM treated culture formed only 1.8 foci of the types II+ III(p<0.05). While MNNG-treated culture formed 13.0 foci, MNNG + 0.2mg/ml alginic acid -SSM treated one produced 3.0 foci of type II+III(p<0.05). These results suggest that alginic acid-SSM can effectively prevent the mutagenicities and also decrease cytotoxicity and transformation induced by some carcinogens.

• Journal of the Korean Society of Food Science and Nutrition
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• v.20 no.2
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• pp.156-161
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• 1991

The mutagenic, comutagenic and antimutagenic effects of red pepper powder were studied by using Ames mutagenicity test. extracts(3 fractions) of the red pepper powder did not show any mutagenicity with or without S9 mix in Salmonella typhimurium strains of TA100 and TA98. These extracts did not show any comutagenicity on N-methyl-N'-nitro-N-nitrosoguanidine(MNNG). Capsaicin also did not exhibit any mutagenicity in the absence or presence of S9 mix prepared from rat or hamster livers. However, the red pepper powder showed antimutagenicity aganist aflatoxin $B_1(AFB_1)$ mediatdd mutagenicity. Especially first fraction of the pepper powder inhibited strongly the mutagenicity of $AFB_1$. There was no difference of these activities between hotter tasted pepper powder and plain hot tasted pepper powder.

• YAKHAK HOEJI
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• v.41 no.4
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• pp.450-455
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• 1997

The preparation of Bacillus coagulans is used as a therapeutics for human intestinal disorders. However, the bacterium in the preparation is very susceptible to rifampic in and fluoroquinolones. When the preparation is taken with rifampicin or fluoroquinolones, its therapeutic effect can not be expected. So B. coagulans RFR17 resistant to rifampicin was obtained by treating the parent B. coagulans with N-methyl-N'-nitro-N-nitrosoguanidine. B. coagulans OFR17 was produced by serial passage of B. coagulans RFR17 on agar with 2-fold minimal inhibitory concentration of ofloxacin or ciprofloxacin. B. coagulans OFR17 was resistant to fluoroquinolones up to 16~64 fold higher than that for the original strain. B. coagulans OFR17 also exhibited identical characteristics with the parent strain when they were tested for lactic acid production and growth inhibition of E. coli MB4-01 and Shigella sonnei MB4-10411. From in vitro test, it was also identified that rifampicin and ofloxacin are not inactivated by certain factors of B. coagulans OFR17. Conclusively, B. coagulans OFR17 can be regarded as a promising strain which can be developed as the preparation for the treatment of the intestinal disorders of the tuberculosis patients under rifampicin and ofloxacin therapy.

• Journal of the Korean Society of Food Culture
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• v.5 no.1
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• pp.169-180
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• 1990

An experimental study on the effect of milk diet on carcinogenesis induced by N-methyl-N-nitro-N-nitrosoguanidine (MNNG) was designed in rats to elucidate its mechanism. A total of 136 Sprague-Dawley rats were divided into 6 groups according to the milk dosagnes in each diet. The entire group of 136 rats was fed the MNNG (100 g/ml) and milk for the initial 28 weeks. Thereafter for the next 12 weeks the group was fed a normal diet only. After this 40 week experiment 109 rats survived. These rats were then dissected with the results being summarized as follows: Suppression of gastroduodenal malignancy was evidenced by the increase of milk concentration in the diet except for the group given MNNG and the lowest concentration of milk (6% milk). Significant differences in the rate of cancer association were present between the regenerative hyperplasia (22.2%) and adenomatous hyperplasia (57.9%). The incidence of benign lesions increased proportionally with the concentration of milk in the diet, especially in regenerative hyperplasia. In the group which had been given the lowest concentration of milk there was a significant increase of the serum gastrin level in the rats with gastric cancer or precancerous benign lesions like regenerative hyperplasia or adenomatous hyperplasia.

• Korean Journal of Food Science and Technology
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• v.21 no.1
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• pp.154-163
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• 1989

This studies were designed to improve the productivity of L-lysine by protoplast fusion and immobilized system of fusants using strains of Brevibacterium flavum ATCC 21528, Brevibacterium lactofermentum ATCC 21086 and Corynebacterium glutamicum 820. Mutants were isolated with concentration method of $300{\mu}g/ml$ penicillin-G after treatment of $250{\mu}g/ml$ N-methyl-N-nitro-N-nitrosoguanidine. B. flavum $37-2(Hos^-,\;Kan^r,\;AEC^r)$, B. lactofermentum $6-2(Ile^-,\;Val^-,\;Str^r,\;AEC^r)$ and C. glutamicum 57-5$(Met^-,\;Thr^-,\;Rif^r,\;AEC^r)$ were isolated from mutants. Protoplasts were induced by being incubated with $500{\mu}g/ml$ lysozyme of lysis solution for 6 hr and the ratio of protoplast formation and regeneration were ranging from 97-99% and 33-37%, respectively. Fusion frequencies of fusants of BBFL 21, BCFG 37 and BCLG 59 were shown in the range from $1.25{\times}10^{-6}\;to\;5.83{\times}10^{-7}$ under the optimum conditions. The fusant BBFL 21 showed the highest productivity of $411.1\;ng/ml{\cdot}hr$ L-lysine in the lysine productivity broth at $30^{\circ}C$ for 72hr. In the immobilization systems, fusant BBFL 21 was employed in various polymer matrices such as sodium alginate, polyacrylamide, agar and ${\alpha}-carrageena$. The immobilization of sodium alginate showed the highest productivity of $413\;ng/ml{\cdot}hr$ L-lysine in the batch system. Continuous fermentation of immobilization system by using tube fermentor was produced the highest productivity $416.7\;ng/ml{\cdot}hr $ L-lysine under optimum condition.

• Journal of the Korean Society of Food Science and Nutrition
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• v.22 no.3
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• pp.307-312
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• 1993

Methanol extract of dried persimmon leaves was fractionated to hexane, chloroform, ethyl acetate, butanol, and aqueous tractions. Hexane, butanol, and aqueous fractions had high yields of extracts. Hexane fraction among these fractions showed the highest inhibition rate on the mutagenicities of aflatoxin (AFB$_1$), dimethyl-amino-bi-phenyl (DMAB), N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), and 4-nitroquinoline-1-oxide (4-NQO) in Salmonella typhimurium TA100. Hexane fraction was further fractionated into eight fractions by silica gel column c-hromatography and thin layer chromatography (TLC). The fraction 5 on TLC exhibited the highest antimutagenic activity on AFB$_1$, DMAB, and MNNC. 1'-oxocannabinol, 3B-acetoxy-17-methyl-5a-18 (13-17) abeoardrost-13-one, 4-methoxy-2'6'-dinitro-3, 5-di-t-butylbiphenyl, 8, 9-dihydro-5, 6-dimethoxy-dibenz ［c, h］isoquino ［2, 1, 8-1 ma］carbazole-11, 16-dione were tentatively identified from this antimutagenic fraction by GC-MS.

• The Korean Journal of Physiology and Pharmacology
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• v.12 no.4
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• pp.185-191
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• 2008

Activation of c-Jun N-terminal kinase (JNK), a member of the mitogen-activated protein kinase family, is an important cellular response that modulates the outcome of the cells which are exposed to the tumor necrosis factor (TNF) or the genotoxic stress including DNA damaging agents. Although it is known that JNK is activated in response to genotoxic stress, neither the pathways to transduce signals to activate JNK nor the primary sensors of the cells that trigger the stress response have been identified. Here, we report that the receptor interacting protein (RIP), a key adaptor protein of TNF signaling, was required to activate JNK in the cells treated with certain DNA damaging agents such as adriamycin (Adr) and 1-${\beta}$-D-arabinofuranosylcytosine (Ara-C) that cause slow and sustained activation, but it was not required when treated with N-methyl-N-nitro-N-nitrosoguanidine (MNNG) and short wavelength UV, which causes quick and transient activation. Our findings revealed that this sustained JNK activation was not mediated by the TNF (tumor necrosis factor) receptor signaling, but it required a functional ATM (ataxia telangiectasia) activity. In addition, JNK inhibitor SP-600125 significantly blocked the Adr-induced cell death, but it did not affect the cell death induced by MNNG. These findings suggest that the sustained activation of JNK mediated by RIP plays an important role in the DNA damage-induced cell death, and that the duration of JNK activation relays a different stress response to determine the cell fate.