• Toxicological Research
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• 제7권2호
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• pp.157-163
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• 1991

The effect of patulin, a mycotoxin, on the growth of Escherichia coli cell was investigated. E. coli cell elongation usually shown in SOS-response for DNA repair was induced by 20 mg of patulin per ml. After staining the E. coli chromosome with fluorescence dye(DAPI, 4', 6-diamino-2-phenyl-indole), chromosomal DNA partitioning was not affected by patulin. The observation indicateds that patulin acts as a DNA damaging agent which is effective for E. coli cell elongation introduced by the inhibition of septum formation.

• 한국환경성돌연변이발암원학회:학술대회논문집
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• 한국환경성돌연변이발암원학회 2004년도 춘계학술대회
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• pp.107-107
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• 2004

• 한국환경성돌연변이발암원학회지
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• 제18권1호
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• pp.43-46
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• 1998

굴(Oester)껍질에 은 이온을 도입해 개발한 수질 정화제 Ag-Os의 복귀 돌연변이원성을 관찰하기 위하여, Salmonella typhymurium TA 1535, TA 1537, TA 98, TA 100 이용하였고, DAN-손상여부를 관찰하기 위하여 Bacillus Subtils H-17($Rec^+$)와 H-45($Rec^-$)을 이용하였다. Ag-Os에 의한 복귀 돌연변이는 관찰되지 않았고, 이는 S9을 첨가시에도 같은 현상을 나타내었다. Rec-assay에 의한 DNA 손상도 관찰되지 않은 결과로 미루어, 수질 정화제 Ag-Os는 본 시험 조건에서 변이원성을 보이지 않음을 확인하였다.

• 약학회지
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• 제36권6호
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• pp.582-590
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• 1992

S. pneumoniae recP mutant was compared with rec-8 mutant to identify whether they are the same gene or not by determining sensitivity to DNA damaging agents. recP and rec-8 mutant have almost same sensitivity to UV, ethylmethane sulfonate, and methylmethane sulfonate, suggesting that recP has the same function as the rec-8 gene in DNA repair.

• Molecular & Cellular Toxicology
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• 제1권2호
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• pp.73-77
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• 2005

Nickel is the one of potent environmental, the occupational pollutants and the classified human carcinogens. It is a serious hazard to human health, when the metal exposure. To prevent human diseases from the heavy metals, it is seemingly important that understanding of how nickel exerts their toxicity and carcinogenic effect at a molecular and a genomic level. The process of nickel absorption has been demonstrated as phagocytosis, iron channel and diffusion. Uptaked nickel has been suggested to induce carcinogenesis via two pathways, a direct DNA damaging pathway and an indirect DNA damaging pathway. The former was originated from the ability of metal to generate Reactive Oxygen Species (ROS) and the reactive intermediates to interact with DNA directly. Ni-generated ROS or Nickel itself, interacts with DNAs and histones to cause DNA damage and chromosomal abnormality. The latter was originated from an indirect DNA damage via inhibition of DNA repair, or condensation and methylation of DNA. Cells have ability to protect from the genotoxic stresses by changing gene expression. Microarray analysis of the cells treated with nickel or nickel compounds, show the specific altered gene expression profile. For example, HIF-I (Hypoxia-Inducible Factor I) and p53 were well known as transcription factors, which are upregulated in response to stress and activated by both soluble and insoluble nickel compounds. The induction of these important transcription factors exert potent selective pressure and leading to cell transformation. Genes of metallothionein and family of heat shock proteins which have been known to play role in protection and damage control, were also induced by nickel treatment. These gene expressions may give us a clue to understand of the carcinogenesis mechanism of nickel. Further discussions on molecular and genomic, are need in order to understand the specific mechanism of nickel toxicity and carcinogenicity.

• Journal of Microbiology and Biotechnology
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• 제16권12호
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• pp.1968-1976
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• 2006

Recombinant E. coli ACV 1003 (recA:: lacZ) was used to measure low concentrations of DNA-damaging chemicals, which produce $\beta$-galactosidase via an SOS regulon system. Very low $\beta$-galactosidase activities of less than 0.01 unit/ml, $\beta$-galactosidase produced through an SOS response corresponding to the 10 ng/ml (ppb) of DNA damaging chemicals in the environment, can be rapidly determined by using an alternative interferometric biosensor with optically flat thin films of porous silicon rather than by the conventional time-consuming Miller's enzyme assay as well as the ELISA method. fu order to enhance the sensitivity in the interferometry, it needs to obtain more uniform distribution and higher biolinking efficiency, whereas interferometric sensing is rapid, cheap, and advantageous in high throughput by using a multiple-well-type chip. In this study, pore size adjusted to 60 nm for the target enzyme $\beta$-galactosidase to be bound on both walls of a Si pore and a calyx crown derivative was apllied as a more efficient biolinker. Furthermore, anti-$\beta$-galactosidase was previously functionalized with the biolinker for the target $\beta$-galactosidase to be specifically bound. When anti-$\beta$-galactosidase was bound to the calyx-crown derivative-linked surface, the effective optical thickness was found to be three times as high as that obtained without using anti-$\beta$-galactosidase. The resolution obtained was very similar to that afforded by the time-consuming ELISA method; however, the reproducibility was still unsatisfactory, below 1 unit $\beta$-galactosidase/ml, owing to the microscopic non-uniform distribution of the pores in the etched silicon surface.

• Animal cells and systems
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• 제2권3호
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• pp.383-388
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• 1998

A RecA-like protein (RecAps) was identified from fluorescent Pseudomonas sp. and the inducible nature of the protein was characterized in detail. It was shown by dose-response and time-course experiments using two DNA damaging agents, nalidixic acid and mitomycin-C, that the cellular level of RecAps protein was increased 3-8 fold compared to that of the control. The most effective doses of nalidixic acid and mitomycin-C for the protein induction were $30{\mu}g/ml$ and $0.3{\mu}g/ml$ at the treatment time point of 150 min, respectively. The enhanced level of RecAps protein was gradually decreased to the control level after 10 hr in normal medium. Interestingly, the cellular level of RecAps protein was increased by the same DNA damaging agents even when cell growth was completely inhibited by treatment with $170{\mu}g/ml$ of chloramphenicol, an inhibitor of protein synthesis, suggesting that new protein synthesis is not required for the induction of RecAps. All these results suggest that a typical S0S repair function driven by RecA-like protein is conserved in Pseudomonas sp. cells as in E, coli.

• 한국환경성돌연변이발암원학회지
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• 제19권1호
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• pp.28-33
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• 1999

The SNF2 family includes proteins from a variety of species with roles I cellular processes such as transcriptional regulation, recombination and various types of DNA repair. Several proteins with unknown function are also included in this family. Here, we report the cloning and characterization of hrp 2+ gene (helicase related gene from S. pombe) which was isolated by PCR amplication using the conserved domain of SNF2 motifs within the ERCC6 gene which encodes a protein involved in DNA excision repair. The hrp2+ gene was isolated by screening with yeast S. pombe genomic library. The isolated cloned contained 6.5 kb insert DNA. Southern blot analysis confirmed that S. pombe chromosome contains the same DNA as hrp2+ gene and this gene exists as a single copy in S. pombe genome. The 4.7 kb transcript of mRNA was identified by Northern blot. To examined the transcriptional regulation of hrp2+ gene, DNA damaging agents were treated. These results indicated that the hrp2+ gene may not be directly involved in DNA replication, but may be involved in damage response pathway.

• 대한한의학회지
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• 제20권1호
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• pp.91-105
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• 1999

The effects of Yinjin and Yinjinsaryongsangagambang on a DNA damaging agent, etoposide-induced apoptosis, cell viability, cell cycle progression, and mRNA expression of apoptosis-related genes of human hepatocyte cell line HepG2 were investigated using tryphan blue exclusion assay, MTT assay, flow cytometry, immunocytometric analysis of PCNA, and quantitative RT-PCR analysis. MTT assay showed that Yinjin and Yinjinsaryongsangagambang increases cellular viability of HepG2 cells in a dosage-dependent manner. Stimulation of cell cycle progression by Yinjin or Yinjinsaryongsangagambang was detected by flow cytometric analysis of the DNA content and immunocytometric analysis of PCNA expression. A significant reduction of a DNA-damaging agent, etoposide-induced apoptosis were found in both Yinjin and Yinjinsaryongsangagambang-treated cells in dosage-dependent manner. In overall, 3-fold reduction of apoptosis was recognized in $10.0\;{\mu}g/ml$ of Yinjin or Yinjinsaryongsangagambang-treated cells compared to untreated cells. Although the difference is not significant, Yinjinsaryongsangagambang showed slightly higher effect on the inhibition of apoptosis than Yinjin. From flow cytometric analysis of apoptosis, while 39.9% of untreated cells showed etoposide-induced apoptotic cell death, only 19.6% or 17.4% of Yinjin or Yinjinsaryongsangagambang-treated cells were fond at apoptotic sub G1 phase, respectively. Interestingly, strong induction of Gadd45-mRNA was observed from Yinjin or Yinjinsaryongsangagambang-treated cells. However, no changes in expression levels of p53 and Waf1 were detected, demonstrating that induction of Gadd45 mRNA expression by Yinjin or Yinjinsaryongsangagambang occurs by p53-independent mechanism. Marked mRNA inductions of two apoptosis-inhibiting genes, Bcl-2 and Bcl- XL, were found in both Yinjin or Yinjinsaryongsangagambang-treated HepG2 cells while no changes was detected in expression levels of an apoptosis-promoting gene, Bax.

• BMB Reports
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• 제36권4호
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• pp.403-408
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• 2003

The relative activities of neutral, cationic, and anionic chromium ascorbate complexes toward isolated human mitochondrial and genomic DNA were investigated at physiologically relevant conditions by agarose gel electrophoresis. A direct relationship between the charge of the Cr(III) species and their DNA-damaging properties was found. The cationic species were found to be fully capable of DNA-cleavage, even in short incubation periods. Incubations were also performed in the presence of amino acids. No apparent effect was observed under the applied experimental conditions to facilitate or prevent damage through the ternary amino acid-Cr-DNA adduct formation or binary chromium-amino acid complex formation.