• 한국동물학회지
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• 제18권1호
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• pp.41-49
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• 1975

DNA 回復合成과 染色體交換과의 聯關性을 추구하기 위해 감마線을 照射한 BHK-21 과KB 細胞의 DNA 回復合成의 線量反應과 時期를 調査하였다. 감마 線에 의한 DNA 回復合成率은 5kR까지 照射線量에 比例하나 그후 50kR 까지는 變化가 없었다. DNA 回復合成의 初期 線量反應은 細胞에 따라 다르나 照射후 1$\\sim$2時間까지 지속하였다. 감마 線에 의한 染色體交換은 細胞에 따라 다른 感受性을 보였고 DNA 回復合成과의 聯關性을 보여주지 않았다.

• 한국동물학회지
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• 제20권1호
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• pp.41-48
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• 1977

Bleomycin에 의해 유발된 DNA 회복합성은 저농도 처리군에서는 농도의 증가에 따라 증가하며 $5\\mu$g/ml 군에서 조사한 전세포의 15%가 회복합성을 하여 최고율을 보인다. 고농도 처리군에서 DNA 회복합성율이 감소하며 처리 시간을 연장해도 그율은 변화가 없다. BUdR이나 IUdR을 전처리한군에서는 DNA회복합성을 증가시키는 것으로 판명됐으며 또한 고동도 처리군에서는 정상적인 DNA 합성을 억제한다. 시간 변화에 따른 실험에서는 처리한 bleomycin을 제거한후 24시간까지 DNA 회복합성이 계속됐다. 이들 결과는 bleomycin이 excision repair를 유발하는 효과적인 화학물질이 아니며, bleomycin에 의해 유발되는 DNA의 손상은 DNA 나선 절단뿐만 아니라 다른 형태의 DNA 손상도 유발함을 추측할수 있다.

• 한국환경성돌연변이발암원학회지
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• 제9권1호
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• pp.23-32
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• 1989

Chinese hamster ovary (CHO)-K1 cells echibited a differential sensitivity in the process of DNA repair synthesis induced by ethyl methanesulfonate (EMS) or bleomycin (BLM) in relation to cell cycle. Two assays were employed in this study: alkaline elution and unscheduled DNA synthesis. The post-treat-ment with aphidicolin (APC), an inhibitor of DNA polymerase alpha, inhibited DNA repair synthesis induced by EMS in G2 phase, while APC did not show any effect on BLM-induced DNA repair synthesis in all phases. On the other hands, the 2', 3'-dideoxythymidine (ddTTP), an inhibitor of DNA polymerase beta, inhibited DNA repair synthesis induced by EMS or BLM in both of G1 and G2 phases. These results suggested that the involvement of DNA polymerase alpha and beta in DNA repair was dependent on cell stage or used chemical agent.

• 한국환경성돌연변이발암원학회지
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• 제11권2호
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• pp.107-117
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• 1991

The effect of 3-aminobenzamide (3AB), an inhibitor of poly (ADP-ribose) polymerase, on ethyl methanesulfonate (EMS)-or bleomycin (BLM)-induced DNA repair synthesis and chromosome aberrations was examined during the cell cycle of Chinese hamster ovary (CHO)-K$_1$ cells. The synchronized cells were obtained by using thymidine double block method and mitotic selection method. Three assays were employed in this study: unscheduled DNA synthesis, alkaline elution and chromosome aberrations. 3AB alone did not induce DNA repair and chromosome aberrations in all phases. The post-treatment with 3AB inhibited DNA repair synthesis induced by EMS or BLM in G$_2$ phase, whereas 3AB did not affect chromosome aberrations induced by EMS or BLM in all phases. These results suggest that 3AB aggravates the cell cycle disturbance which occur after DNA damage, and leads to an accumulation of cells at G$_2$ phase, and inhibits DNA repair synthesis, while the effect 3AB on chromosome aberrations may need reevaluated.

• 한국동물학회지
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• 제20권2호
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• pp.93-99
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• 1977

HeLa $S_3$세포에서 MMC에 의해 유발된 DNA회복합성은 농도$(0.05\\sim 0.5\\mu g/ml)$에 따른 증가를 보이지 않고 그 율도 비\ulcorner적 낮아 $0.1\\sim 0.5\\mu g/ml$ 농도에서 조사한 전 세포의 $7\\sim 9%$를 나타내고 있다. 시간 변화에 따른 실험에서는 MMC를 제거한 후 24시간까지 거의 비슷한 율로 DNA회복합성이 계속되고 있다. thymidine 상사체중 BUdR을 전처리한 군에서만이 MMC에 의한 DNA회복합성을 증가시켰다. 그러나 BUdR 또는 IUdR과 MMC를 복합처리 할 경우 시간경과에 따라 정상 DNA합성은 감소된다. 이들 결과는 MMC에 의해 유발된 DNA손상은 빠르고 느린 두단계로 회복됨을 암시하는 것이라 생각된다.

• Journal of Ginseng Research
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• 제16권3호
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• pp.210-216
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• 1992

The effect of saponin extracted from Panax grneng CA Meyer on DNA repair and replicative DNA synthesis were examined in CHO-Kl cells cotreated with benzo(a)pyrene and rat liver S-15 fraction. The DNA strand breaks inititated by benzo(a)pyrene metabolites were measured by alkaline election technique. The addition of ginseng saponin to the culture media resulted in decrease of benzo(a)pyrene-induced DNA strand breaks, and restored the suppressed-semiconservative-DNA-synthesis by the carcinogen. DNA repair synthesis in the damaged cells was also elevated by the ginseng treatment when the repairing activites were measured for the (3H)-thymidine incorporation into the carcinogen damaged cellular DNk Comparative analysis of DNA-adduces of benzo(a)pyrene metabortes in microsomes suggested that ginseng saponin treatment in rats reduced the formation of electrophilic metabolites of benzo (a)-pyrene in the rat liver microsomes.

• Toxicological Research
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• 제34권4호
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• pp.297-302
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• 2018

Cells are constantly exposed to endogenous and exogenous chemical and physical agents that damage their genome by forming DNA lesions. These lesions interfere with the normal functions of DNA such as transcription and replication, and need to be either repaired or tolerated. DNA lesions are accurately removed via various repair pathways. In contrast, tolerance mechanisms do not remove lesions but only allow replication to proceed despite the presence of unrepaired lesions. Cells possess two major tolerance strategies, namely translesion synthesis (TLS), which is an error-prone strategy and an accurate strategy based on homologous recombination (homology-dependent gap repair [HDGR]). Thus, the mutation frequency reflects the relative extent to which the two tolerance pathways operate in vivo. In the present paper, we review the present understanding of the mechanisms of TLS and HDGR and propose a novel and comprehensive view of the way both strategies interact and are regulated in vivo.

• 한국환경성돌연변이발암원학회지
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• 제9권1호
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• pp.13-22
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• 1989

The effect of novobiocin (NOV), and inhibitor of topoisomerase II, on ethyl methanesulfonate (EMS)-or bleomycin (BLM)-induced DNA repair synthesis was examined during the cell cycle of Chinese hamster ovary (CHO)-K1 cells. Three assays were employed in this study: cell survival, alkaline elution and unscheduled DNA synthesis. EMS was effective at killing CHO cells in G1 phase, wheras BLM preferentially killed cells in G2 and S phases. EMS induced the much more amount of DNA damage in G1 phase, while BLM induced in G2 phase than the other phases. The both of pre- and post-treatment with BOV inhibitied EMS- or BLM-induced DNA repair synthesis in G1 and G2 phases, and pretreatment with NOV inhibited more effectively than the post-treated group. These results suggested that CHO cells exhibited a differential sensitivity to cell lethality and DNA damage in relation to cell cycle according to used chemical agents, and that DNA topoisomerase II participated in an initial stage of DNA repair.

• 대한의생명과학회지
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• 제11권2호
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• pp.103-108
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• 2005

2-Deoxyribonolactone (dL) arises as a major DNA damage induced by a variety of agents, involving free radical attack and oxidation of C1'-deoxyribose in DNA. We investigated whether dL lesions can be repaired in mammalian cells and the mechanisms underlying the role of DNA polymerase $\beta$ in processing of dL lesions. Pol $\beta$ appeared to be trapped by dL residues, resulting in stable DNA-protein cross-links. However, repair DNA synthesis at site-specific dL sites occurred effectively in cell-free extracts, but predominantly accompanied by long-patch base excision repair (BER) pathway. Reconstitution of long-patch BER demonstrated that FEN1 was capable of removing the displaced flap DNA containing a 5'-dL residue. Cellular repair of dL lesions was largely dependent on the DNA polymerase activity of Pol $\beta$. Our observations reveal repair mechanisms of dL and define how mammalian cells prevent cytotoxic effects of oxidative DNA lesions that may threaten the genetic integrity of DNA.

• 약학회지
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• 제36권5호
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• pp.449-454
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• 1992

The effect of radioprotective ginseng protein fraction on DNA repair capacity was determined by measuring the amount of $^{3}H-thymidine$ incorporated into DNA in the process of repair synthesis for UV damaged DNA. CHO-Kl cells were prepared whose semiconservative replication was inhibited by trimethylpsoralen plus near-UV(PUVA) treatment. When the cells were exposed to UV light alone, the DNA repair capacity was increased at first and then decreased as UV dose increased. However, when the ginseng fraction was treated to the cells, the DNA repair capacity was kept increasing regardless of UV dose increment. When the concentration of protein contained in the added fraction was increased gradually, the repair capacity was also increased almost linearly showing dose-response relationship of the effect. These results suggest that the enhancement of DNA repair capacity of the cell can be one of the mechanisms of radioprotection by the ginseng fraction.