• Proceedings of the Korean Society of Life Science Conference
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• 2001.02a
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• pp.73-73
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• 2001

• Journal of Microbiology and Biotechnology
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• v.14 no.2
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• pp.268-275
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• 2004

To investigate the potential application of the single-cell gel electrophoresis (SCGE) assay to carp as an aquatic pollution monitoring technique, gill, liver, and blood cells were isolated from carp exposed to a direct-acting mutagen, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), or indirect mutagen, $benzo[\alpha]pyrene$ $(B[\alpha]P)$, then the DNA strand breakage was analyzed using the assay. Based on testing 5 different cell isolation methods and 6 electrophoretic conditions, the optimized assay conditions were found to be cell isolation by filter pressing and electrophoresis at a lower voltage and longer running time (at 0.4 V/cm for 40 min). In preliminary experiments, gill and liver cells isolated from carp exposed to MNNG in vitro exhibited DNA damage signals even with 0.5 ppb exposure, which is a much higher dose than previously reported. In the gill cells isolated from carp exposed to 0.01-0.5 ppm MNNG in vivo, significant dose-and time-dependent increases were observed in the tail for 4 days. As such, the linear correlation between the relative damage index (RDI) values and time for each dose based on the initial 48-h exposure appeared to provide effective criteria for the genotoxicity monitoring of direct-acting mutagenic pollution. In contrast, the in vivo exposure of carp to 0.25-1.0 ppm of $B[\alpha]P$ for 7 days resulted in dose-and time-dependent responses in the liver cells, in which 24-h delayed responses for metabolizing activation and gradual repair after 48 h were also observed. Thus, the negative-sloped linear correlation between the RDI and time at each dose based on the initial 48 h appeared to provide more effective criteria for the genotoxicity monitoring of indirect mutagenic pollution.

• The Korean Journal of Zoology
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• v.23 no.3
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• pp.115-123
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• 1980

The rates of escision repair at various doses and times after MNNG treatment in CHO cells were compared with the frequencies of chromosome aberrations to determine a possible relation between there two types of biological phenomena, and the results obtained were as follows: 1. the MNNG-induced excision repair was dose-dependent in te ranges between $0.5 \\times 10^-5$M. The maximum rate of excision repair was occurred in the cells soon after the treatment. The rates were then gradually decreased and appeared about 66% of 0 hour at 24 hours. 2. The rates of chromosome aberrations induced by MNNG was the highest at 6 hours, in which majority were chromatid deletions. The rates of chromatid deletions decreased, whereas chromatid exchanges increased with time, resulting is about equal rates at 24 hours after treatment. 3. The rates of excision repair at different times after MNNG treatment were roughly related to the total breaks per cell. The rates, however, did not show any relation to either chromatid exchanges or deletions. These results may suggest that excision repair may not be directly related to chromosome aberrations in MNNG treated CHO cells.

• Archives of Pharmacal Research
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• v.11 no.3
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• pp.225-229
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• 1988

A ginseng protein fraction which has been reported to have radiation protective effect was purified from Korean ginseng and its effects on relative survival and chromosome aberration were studied in UV irradiated CHO-K1 cells. When the protein fraction $(100\;{\mu}g/ml)$ was added to the cells before UV irradiation at 4\;J/$m^2$,, the survival rates were increased to 53.8% from 40.6% in control. Addition of the protein $(100\;{\mu}g/ml)$ after UV irradiation at 4 and $8\;J/m^2$ raised the rates to 85.4 and 24.0% from 79.2 and 11.5% in control, respectively. When the ginseng protein $(800\;{\mu}g/ml)$ was added to the cells exposed to UV light at 10, 20, $30\;J/m^2$, the frequencies of chromosome aberration (CA) were reduced significantly to almost same level regardless of the UV dose increment and there was no significant difference between pre- and post-treatment. When the concentration of ginseng protein was increased from 200 to $800\;{\mu}g/ml$, at UV dose of 10, 20, $30\;J/m^2$ each, the CA frequencies were decreased consistently as the dose of ginseng protein increased, at all UV doses tested. Similar effects were observed in both cases of pre- and post-treatment. The data suggest that the protein may reduce cell damage caused by UV light, especially damage to DNA molecule, or play a role in repair processes of damaged DNA, to increase cell survival and reduce chromosome aberrations.

• BMB Reports
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• v.46 no.2
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• pp.113-118
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• 2013

TTRAP is a multi-functional protein that is involved in multiple aspects of cellular functions including cell proliferation, apoptosis and the repair of DNA damage. Here, we demonstrated that the lentivirus-mediated overexpression of TTRAP significantly inhibited cell growth and induced apoptosis in osteosarcoma cells. The ectopic TTRAP suppressed the growth and colony formation capacity of two osteosarcoma cell lines, U2OS and Saos-2. Cell apoptosis was induced in U2OS cells and the cell cycle was arrested at G2/M phase in Saos-2 cells. Exogenous expression of TTRAP in serum-starved U2OS and Saos-2 cells induced an increase in caspase-3/-7 activity and a decrease in cyclin B1 expression. In comparison with wild-type TTRAP, mutations in the 5'-tyrosyl-DNA phosphodiesterase activity of TTRAP, in particular $TTRAP^{E152A}$, showed decreased inhibitory activity on cell growth. These results may aid in clarifying the physiological functions of TTRAP, especially its roles in the regulation of cell growth and tumorigenesis.

• Journal of Convergence for Information Technology
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• v.11 no.2
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• pp.201-210
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• 2021

This study was carried out to investigate the Fagopyrum esculentum (F. esculentum) extracts and vitexin are as the results of microarray, cell proliferation, cell wound recovery, cell cycle, microphage pattern and protein analysis for damage improvement caused by UVB-induced damage. Microarray results showed that UVB-induced increase in DRAM1, Atg2a and Atg13 genes was reduced in F. esculentum ethanol extract and vitexin. Cell proliferation, wound repair, cell cycle, and microphage patterns were improved in F. esculentum ethanol extract and vitexin, while buckwheat ethanol extract and vitexin decreased in both DRAM1, Beclin-1, and LC3 I/II in the vitexin treatment group and p-mTOR and survivin were all increased in protein analysis. It is thought that it can recover to normal and control autophagy, one of the causes of cell aging caused by UVB, to inhibit and regenerate cell death. F. esculentum ethanol extract and vitexin can be used as a functional cosmetic ingredient.

• Journal of radiological science and technology
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• v.34 no.4
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• pp.333-339
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• 2011

The purpose of this study is to compare DNA repair characteristics of normal fibroblast cell (MRC-5) and neuroblastoma cell (SK-N-SH) induced by proton beam. Cells were irradiated with 2Gy, 5Gy and 8Gy proton beam. The rate of DNA rejoining was measured by alkaline version of the comet assay. After a repair time, tail moment was measured again. The tail moment of MRC-5 was lower than SK-N-SH. However, after 8Gy of exposure, the tail moment of MRC-5 was measured as 50.320223.17155 which represents dangerous level of DNA damage. The cells were repaired practically within 25 hours after 2 and 5Gy of exposure while they were not fully recovered after 8Gy of exposure. Especially, tail moment of MRC-5 after 25 hours was 18.15364.42849. In the distal declining edge of SOBP, the RBE value is increased by high LET. The RBE differences of SOBP in high-dose were greater than low-dose. After the high-dose exposure, MRC-5 of normal fibroblast cell could lead to lasting DNA damage as shown in this study. In conclusion, we has to pay special attention when the region of the treatment volume is close to sensitive tissues.

• Journal of Veterinary Clinics
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• v.21 no.3
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• pp.253-258
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• 2004

DNA double-strand break (DSB) is a serious treat for the cells including mutations, chromosome rearrangements, and even cell death if not repaired or misrepaired. Ku heterodimer regulatory DNA binding subunits (Ku70/Ku80) bound to double strand DNA breaks are able to interact with 470-kDa DNA-dependent protein kinase catalytic subunit (DNA-PKcs), and the interaction is essential for DNA-dependent protein kinase (DNA-PK) activity. The Ku80 mutants were designed to bind Ku70 but not DNA end binding activity and the peptides were treated in breast cancer cells for co-therapy strategy to see whether the targeted inhibition of DNA-dependent protein kinase (DNA-PK) activity sensitized breast cancer cells to ionizing irradiation or chemotherapy drug to develop a treatment of breast tumors by targeting proteins involved in damage-signaling pathway and/or DNA repair. We designed domains of Ku80 mutants, 26 residues of amino acids (HN-26) as a control peptide or 38 (HNI-38) residues of amino acids which contain domains of the membrane-translocation hydrophobic signal sequence and the nuclear localization sequence, but HNI-38 has additional twelve residues of peptide inhibitor region. We observed that the synthesized peptide (HNI-38) prevented DNA-PKcs from binding to Ku70/Ku80, resulting in inactivation of DNA-PK complex activity in breast cancer cells (MDA-465 and MDA-468). Consequently, the peptide treated cells exhibited poor to no DNA repair, and became highly sensitive to irradiation or chemotherapy drugs. The growth of breast cancer cells was also inhibited. These results demonstrate the possibility of synthetic peptide to apply breast cancer therapy to induce apoptosis of cancer cells.

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.114-114
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• 2003

p53 has identified as a tumor suppressor protein to protect cells from DNA damage. p53, also well known for a transcription factor, can activate genes such as p21, bax, gadd45 and induce a number of the responses such as differentiation, senescence, DNA repair, apoptosis and the inhibition of angiogenesis to protect cells. Many mechanisms of p53 activation have been studied.(omitted)

• CELLMED
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• v.3 no.3
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• pp.25.1-25.8
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• 2013

Homoeopathically prepared Condurango 30C is traditionally used in amelioration of certain types of cancer by homeopathic practitioners. In this study, ability of Condurango 30C in amelioration of the conventional benzo[a]pyrene (BaP)-induced lung cancer in rat has been tested. After one month of scheduled oral feeding of BaP, lung cancer is routinely developed after four months in rats. Tumorbearing rats were then treated with Condurango 30C for the next one ($5^{th}$), two ($6^{th}$) and three ($7^{th}$) months, respectively, and sacrificed. Efficacy of post-cancer treatment by Condurango 30C was evaluated against controls (placebo) by different study parameters like: body and lung weights, number and diameter of lung tumour nodules, lung architecture, DNA damage, anti-oxidant activity and reactive oxygen species (ROS) accumulation. Administration of this homeopathic remedy caused increase of body weight and decrease of lung weight, decrease in number and diameter of lung tumour nodules, particularly after one and two months of drug treatment. BaP intoxication significantly increased lipid peroxidase (LPO) with concomitant decrease in activities of different antioxidants, while Condurango 30C administration certainly reduce their levels than normal and cancerous groups, notably after one and two months' of drug treatment. Condurango 30C showed capability to induce ROS-mediated cell death evidenced from the study of ROS activities at different time-points. Further, the remedy possibly achieved its anticancer goal through mediation of DNA-nicks that possibly led cancer cells to the apoptotic pathway. Thus, Condurango 30C has anticancer potential in BaP-induced lung cancer of rats via tissue damage recovery and ROS-mediated programmed cell death.