• Environmental Mutagens and Carcinogens
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• v.16 no.2
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• pp.117-123
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• 1996

This study was carried out to examine the mechanism of Arsenic cytotoxicity through several in vitro test systems. Dose-dependent decrease of cell survival by Arsenic was observed by colony forming assay. Arsenic was weak mutagenic in inducing HGPRT point mutation in CHO cells. The frequency of chromosomal aberrations increased in a dose-dependent manner and the most frequent type of chromosomal aberrations induced by Arsenic were chromatid type deletions. U!trafiltrates of culture media from CHO cells treated with Arsenic induced sister chromatid exchanges(SCE) in CHO cells and Arsenic was able to induce lipid peroxidation in CHO cells. The results suggested that the ultrafiltrates of media from CHO cells treated with Arsenic contain clastogenic factor(CF) and Iipid peroxidation might be involved in the formation of CF.

• Journal of Nutrition and Health
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• v.27 no.3
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• pp.253-262
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• 1994

This study was intended to investigate the anticarcinogenic effect of ginseng previously elucidated by other researches in animal studies. The sister chromatid exchange(SCE) method of human lymphocytes was used as a biomarker. Based on the literature search and the results of our laboratory, smoking was used as a parameter elevating the SCE frequency of general human population. To evaluate the smoking and ginseng effect on SCE frequency, 98 male healthy factory workers aged 23 to 58 years were divided into 4 groups : smoker with ginseng (SG), smoker control(SC), non-smoker with ginseng(NSG), and non-smoker control(NSC) groups, according to their smoking habits and ginseng intake. The mean sponteneous SCE per cell for the SG(10.8$\pm$0.3) and SC(10.4$\pm$0.3) groups were significantly higher than the NSG(9.1$\pm$0.2) and NSC(9.3$\pm$0.3) groups(p<0.05). High frequency cells (HFCs, cells with 15 SCEs) in SG and SC groups were also greater than those in NSG and NSC groups. However, the SCE levels of the SG and SC groups were not associated with the personal smoking history and the number of cigaretts smoked per day. Ginseng intake did not show any effect on the increased SCE caused by smoking. There were no correlations of the elevated SCE among smoking and ginseng types, history of ginseng intake, and consumption frequencies of ginseng intake. These results does not support the findings of other researchers that ginseng could be a protective agent to DNA damage.

• Journal of Radiation Protection and Research
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• v.27 no.2
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• pp.81-87
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• 2002

The interaction of low density extremely low frequency magnetic field (ELF MF) in the frequency of hypoxanthine-guanine phosphoribosyltransferase (HPRT) mutation induced by bleomycin and on the frequency of sister chromatid exchanges (SCEs) induced by 1,2,4-benzenetriol(BT) was demonstrated. CHO cells pretreated with bleomycin or 1,2,4-benzenetriol were exposed for 24hrs to a sinusoidal 0.8mT magnetic field at 60Hz. Frequency of HPRT mutation and SCEs were determined. ELF MF exposure led to a two-fold increase of the frequency of HPRT mutation induced by bleomycin. No increase of mutation frequency was observed by ELF MF alone ELF MF also increased the frequency of SCEs induced by BT while no Increase of SCE frequencies were observed by ELF MF alone. These results suggest that low density ELF MF field would art as an enhancer rather than as an initiator of mutagenic effects in CHO cell.

• YAKHAK HOEJI
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• v.39 no.1
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• pp.94-101
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• 1995

In order to evaluate the suppressive effects of galangin on the DNA damage induced by N-methyl-N-nitrosourea(MNU), in vitro sister chromatid exchange(SCE) test using Chinese Hamster ovary(CHO) cells was performed. Also the determinations of [$^{3}$H] MNU-induced total DNA binding and methylated DNA were performed to find out the mechanism of action by galangin. MNU-induced SCEs were significantly decreased by simultaneous and pretreatment of galangin when S-9 mix was added only. In post-treatment, however, the MNU-induced SCEs were not decreased when S-9 mix was added or not. [$^{3}$H] MNU-induced total DNA binding was significantly inhibited by the treatment of galangin in calf thymus DNA and CHO cells. HPLC analysis of DNA hydrolysates shows that galangin caused a dose-dependant decrease in calf thymus DNA, but not significant decrease in CHO cells. These results suggest that the inhibition of galangin on the MNU-induced SCEs is due to the decrease of DNA binding and methylation with MNU. Therefore, galangin may be useful as a chemopreventive agent of alkylating agents.

• Archives of Pharmacal Research
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• v.11 no.2
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• pp.93-98
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• 1988

To elucidate the reaction mechanism of ginseng protein on its antiradiation activity, its effects were studied on sister chromatid exchanges (SCE) induced by UV irradiation in CHO-KI cells. When cells were irradiated with 254 nm UV light at the dose of 0 to 8erg$\textrm{mm}^2$, the frequencies of CSE were increased more than two fold. However, when radio protective ginseng protein was added to the cells before the after UV irradiation, SCE frequencies were decreased significantly at all UV doses in both cases with no significant differences. As the amount of ginseng protein was varied from 100 to 500 .mu.g/ml, with UV irradiation at 60 erg$\textrm{mm}^2$, SCE frequencies dropped sharply at the first two concentrations and then reached a sort of plateau in both cases of pre-and post-treatment. When the ginseng protein was treated alone without UV irradiation, there were no changes in SCE frequencies no matter when the protein was added. There results suggest that the ginseng protein could reduced DNA damages, which may play an important role in the reaction mechanism of radioprotective activity of the protein.

• Journal of Preventive Medicine and Public Health
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• v.17 no.1
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• pp.245-250
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• 1984

Reciprocal exchanges of DNA in sister chromatids (SCEs) are induced by various carcinogens and mutagens, although the quantitative relationship between the number of mutations and SCEs induced varies among chemicals. Nevertheless, the analysis of SCEs production by various agents often proposed as a sensitive and quantitative assay for mutagenicity and cytotoxicity. Mercury, even if which has no evidences for mutagenicity and carcinogenicity, is reported to exert some cytotoxic effects, such as chromosomal aberrations or bad influences to ovulation and reproduction in experimental animals, etc.. In this study, tests for sister chromatid exchanges have been carried out on normal human lymphocytes in whole blood culture to add mercury chloride ($HgCl_2$) or methylmercury chloride ($CH_3\;HgCl$) for 72 hr. The results indicate the dose-dependent relationship between the frequencies of SCEs and the concentrations of $HgCl_2,\;CH_{3}HgCl$ and 5-bromo-2'-deoxyuridine (BrdU). Lymphocyte proliferation has depressed in the higher concentration of mercury.

• 대한예방의학회:학술대회논문집
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• 1995.10a
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• pp.351-352
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• 1995

• The Korean Journal of Zoology
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• v.23 no.4
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• pp.203-218
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• 1980

Unscheduled DNA synthesis, chromosome aberrations, sister chromatid exchanges and DNA replication inhibition induced by the combined treatments with ara-C and UV-light or MMS in $HF_1$, CHO and $HelaS_3$ cells were studied, and the results obtained were as follows: (1) Ara-C was found to inhibit UV-or MMS-induced unscheduled DNA synthesis and the inhibitory effect of ara-C was more remarkable in its post-treatment. (2) Ara-C enhanced the rate of chromosome aberrations induced by MMS or UV-light. Post-treatment with ara-C exhibited the synergistic effect on MMS-induced chromosome aberrations mainly by increases of chromatid deletions. (3) Contrarily, ara-C did not increase the rate of sister chromatid exchanges, particularly in the pre-treatment with MMS, although it was found to induce sister chromatid exchanges. (4) The rate of DNA synthesis was declined immediately after are-C treatment and then recovered. The combined treatments with ara-C and UV-light or MMS showed that the initial response on replication inhibition was similar to that of ara-C, but later responses were similar to that of UV-light or MMS treated group.

• Toxicological Research
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• v.11 no.1
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• pp.117-125
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• 1995

In order to examine the mechanism of asbestos clastogenicity, CHO cells were treated with chrysotile and crocidolite. Crocidolite and chrysotile were able to induce lipid peroxidation in a dose dependent manner. Ultrafiltrate of culture media from CHO cells treated with chrysotile/crocidolite induced sister chromatid exchange in CHO cells. Ultrafiltrate of culture media from CHO cells treated with chrysotile induced chromosome aberration but it was not statistically significant. Simultaneous treatment of 3-Aminobenzamide (3-AB) or cytosine arabinoside (Ara C) with crocidolite had no effect on the frequency of chromosome aberration by crocidolite whetease posttreatment of caffeine significantly increased the chromosomel aberration by crocidolite. This indicated that DNA damage by asbestos took place at late stage of cell cycle. The results suggested that the ultrafiltrate of media contained clastogenic factor (CF) and lipid peroxidation might be involved in the formation of CF.

• Journal of Food Hygiene and Safety
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• v.11 no.2
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• pp.115-121
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• 1996

In order to compare the suppressive effect of quercetin and several its glycosides, such as quercitrin (quercetin-3-rhamnoside), isoquercitrin (quercetin-3-glucoside), hyperin (quercetin-3-galactoside) and tutin (quercetin-3-rhamnosyl glucoside), on the genotoxicity by N-methyl-N-nitrosourea(MNU), in vitro sister chromatid exchange(SCE) test using mouse spleen lymphocytes and in vivo micronucleus test using mouse peripheral blood were performed. MNU-induced SCEs in vitro were not decreased by the simultaneous treatment of test compounds. Among them, quercetin and hyperin showed significant suppressive effects at high dose(10-5M). On the other hand, MNU-induced micronucleated reticulocytes(MNRETS) in vivo were significantly decreased with good dose-dependent manner in all compound tested. However, there were not significant differences between quercetin aglycone and its glycosides in the suppressive aglycone and its glycosides may act as an antigenotoxic agent in vivo and may be useful as a chemopreventive agent of alkylating agent.