• 대한예방의학회:학술대회논문집
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• 1995.10a
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• pp.319-320
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• 1995

• Journal of Preventive Medicine and Public Health
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• v.29 no.3 s.54
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• pp.597-607
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• 1996

Genotoxic agents can induce various DNA lesions. DNA-Protein Crosslinks(DPCs) were known as the important DNA lesions which could impair gene expression because DPCs had a high probability of resisting repair and persisting through cell cycle. This repair resistance of DPCs could have biological significance but had not been evaluated clearly yet. Most of the studies that have evaluated the repair of DPCs only compared the extent of DPCs repair with other DNA lesions. We injected $K_2CrO_4$, a genotoxic agent, into Sprague-Dawley rats intraperitoneally(5mg/kg) and isolated blood lymphocytes 12 hours later. These lymphocytes were cultured in the mitogen added growth media and mitogen free media separately. The degree of the repair of DPCs was monitored for 4 days by the K-SDS assay. 4 days later, the amount of DPCs decreased by 4.6% in the mitogen added media high increased by 10.9% in the mitogen free media. These results showed that DPCs induced by $K_2CrO_4$ were not repaired easily and the DPCs were biologically significant DNA lesions. We thought the decrease of DPCs in the mitogen added media was not due to the repair of DPCs, but from the increase of normal cell proliferation. Therefore, it is very important to consider the proliferation of normal cells when estimating the repair of DPCs.

• 대한예방의학회:학술대회논문집
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• 1996.10a
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• pp.275-276
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• 1996

• Environmental Mutagens and Carcinogens
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• v.19 no.1
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• pp.20-27
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• 1999

In order to know the inhibitory effect of magnesium carbonate(MgCO3) on cytotoxicity, DNA damage, mutagenicity, and cell transforming ability of nickel subsulfide, the inhibition of cell proliferation, DNA-protein crosslinks formation (DPC), HGPRT point mutation, and cell transformation were evaluated. Nickel subsulfide(Ni3S2) and magnesium carbonate as insoluble compounds were used for this study. BALB/3T3 cell, CHO-K1 cell, and C3H10T1/2 cell were used in this experiment. Exposure concentration of nickel subsulfide was 1 $\mu\textrm{g}$/ml. The concentrations of magnesium carbonate in this study were 0.6 $\mu\textrm{g}$/ml, 1.2 $\mu\textrm{g}$/ml, 2.4 $\mu\textrm{g}$/ml and the molar ratio of magnesium to nickel when exposed simultanously were 0.5, 1.0 and 2.0 respectively. The results were as follows; 1. Magnesium carbonate reduced the inhibitory effect of nickel subsulfide on cell proliferation. 2. Magnesium carbonate also reduced the effect of nickel subsulfide on DNA-protein crosslinks formation. 3. HGPRT point mutagenicity of nickel subsulfide was reduced when magnesium carbonate treated simultaneously. 4. Magnesium carbonate reduced cell transforming ability of nickel subsulfide. Conclusively, nickel subsulfide showed cytotoxicity, cell transforming ability, and mutagenicity strongly and magnesium carbonate may have protective roles in these nickel effects.

• The Korean Journal of Zoology
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• v.26 no.1
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• pp.19-28
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• 1983

Alkaline elution profiles showed that the frequency of DNA single strand breaks associated with DNA-protein crosslinks in cells treated with both an inducing dose of MMC $(MMC_1)$ and a challenge dose of MMC $(MMC_2)$ was slightly less than that in cells treated with MMC alone. The amount of unscheduled DNA synthesisi in cells treated with both $MMC_1$ and $MMC_2$ was greater than that in cells treated with MMC alone. This enhancement of exicision repair detected by UDS autoradiography and alkaline elution, was not observed, when cells were incubated with cyclohexmide between the two treatments of $MMC_1$ and $MMC_2$. These results suggest that MMC-damaged DNA from Chinses hamster cells is repaired by excision repair mechanisms that require de novo protein synthesis for enhancement, and that an inducible repair mechanism may exist in CHO cells.

• Journal of Life Science
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• v.10 no.6
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• pp.621-629
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• 2000

Camptothecin (CPT) is an antitumor alkaloid that has been isolated from the Chinese tree, Camptotheca acuminata. The cytotoxicity of CPT has been correlated to its inhibition of DNA topoisomerase (Topo) I by stabilizing drug-enzyme-DNA “cleavable complex" resulting in DNA single-strand breaks and DNA-protein crosslinks. This studies were designed to elucidate whether CPT regulates Topo I mediated by CPT in DNAs containing c-myc protooncogene. We have conducted experiments on Topo I purification, pUC-MYC I cloning and Topo I assay using electrophoresis, quantitative RT-PCR and Northern blotting techniques. CPT ingibited the relaxation activity of Topo I in pUC19 DNA at various concentrations (1-1000 $\mu$M), while it enhanced the cleavage of Topo I in the pUC-MYC I by forming a cleavable complex at relatively high concentrations (100-1000 $\mu$M). In HL-60 cells treated with CPT, the expression of c-myc gene was decreased over that in the control group with no changes in the expression of Topo I mRNA. Our results suggest that Topo I is the target of CPT cytotoxicity but it does not affect Topo I extression, and the suppression of c-myc mRNA expression by CPT is due to c-myc damage resulted from formation of a cleavable complex with CPT. CPT.

• 대한예방의학회:학술대회논문집
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• 1998.10b
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• pp.60-61
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• 1998