• 대한예방의학회:학술대회논문집
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• 대한예방의학회 1995년도 제47차 추계 학술대회 연제집
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• pp.319-320
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• 1995

• Journal of Preventive Medicine and Public Health
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• 제29권3호
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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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• 대한예방의학회 1996년도 제48차 추계 학술대회 연제집
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• pp.275-276
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• 1996

• 한국환경성돌연변이발암원학회지
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• 제19권1호
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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.

• 한국동물학회지
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• 제26권1호
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• pp.19-28
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• 1983

본 연구는 알킬화제이며 항암항생제인 Mitomycin C(MMC)와 Bleomycin(BLM)이 DNA 복제 및 회복에 미치는 영향을 규명하고, 아울러 MMC에 의한 "유발상해회복"이 포유동물세포에 유발되는지 밝히고자 수행하였다. 이를 위해 자기방사법에 의한 비주기 DNA 합성율과 알카리 유출법에 의한 DNA단사절단율을 측정하였다. CHO세포에 MMC를 제 1차 $(MMC_1)$ 처리한 후 5시간 뒤에 제 2차 $(MMC_2)$로 처리하여 얻은 결과는 다음과 같았다. 1. BLM은 비주기 DNA합성을 매우 적게 유발시켰으며, BLM $5\\mug/ml$의 농도에서 부터 비주기 DNA합성율은 증가를 보이지 않았다. BLM은 처리후 1.5시간까지 DNA합성억제를 보였으며, 1.5시간후 DNA합성율이 증가되었으나, 대조군의 60% 수준까지 회복되었을 뿐이다. 2. MMC에 의해 유발된 비주기 DNA합성은 농도에 따라 비례하였으며, 배양후 시간의 간격에 따라 비례하여 감소하였다. 제 1,2차 MMC를 처리한 세포의 비주기 DNA합성은 제 1차만 처리한 세포의 비주기 DNA합성보다 많았다. 3. 알카리 유출법 결과는 MMC에 의하여 유발된 DNA 단백질 연결로 인한 DNA 단사절단율이 농도에 비례함을 나타내었다. DNA 단백질 연결로 인한 DNA 단사절단율은 배양후의 시간에 비례해서 감소되었다. 이러한 결과는 MMC와 BLM 모두가 DNA 상해제임과 MMC에 의한 DNA 상해 부위의 복제율이 어떠한 유발기작에 의하여 촉진됨을 시사한다.촉진됨을 시사한다.

• 생명과학회지
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• 제10권6호
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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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• 대한예방의학회 1998년도 제50차 추계 학술대회 연제집
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• pp.60-61
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• 1998