• Journal of Radiation Protection and Research
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• v.36 no.4
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• pp.190-194
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• 2011

After the first report that electrons with sub-ionization energy of DNA could cause single strand breaks or double strand breaks to DNA, there have been various studies to investigate the mechanisms of DNA damage by low-energy electrons. In this paper, we examined the possibility of using X-ray photoelectron spectroscopy (XPS) to analyze the dissociation patterns of the molecular bonds by electron irradiation on DNA thin films and tried to establish the method as a general tool for studying the radiation damage of biomolecules by low energ yelectrons. For the experiment, pBR322 plasmid DNA solution was formed into the films on tantalum plates by lyophilization and was irradiated by 5-eV electrons. Un-irradiated and irradiated DNA films were compared and analyzed using the XPS technique.

• BMB Reports
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• v.30 no.3
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• pp.188-193
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• 1997

Membrane lipid peroxidation processes yield products that may react with DNA to cause mutations. Lipid hydroperoxides from linoleic acid in the presence of transition metal ions caused strand breaks in plasmid DNA. DNA damage induced by reactive aldehydes known to be produced by decomposition of lipid hydroperoxides, such as 4-hydroxynonenal or rnalondialdehyde, was repaired by endonucleases and exonuclease III which resulted in the increase of single strand breaks in DNA. Lipid hydroperoxides as well as malondialdehyde and 4-hydroxynonenal also caused mutations in the pUC18 lacZ' gene when measured as a loss of ${\alpha}-cornplementation$. In conclusion. the lipid peroxidation could be an important intermediary event in DNA damage and mutation by oxidative stress.

• Environmental Mutagens and Carcinogens
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• v.22 no.3
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• pp.164-168
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• 2002

Phthalate analogues are a plasticizer and solvent used in industry and were reported to be a potential carcinogen classified in the category of suspected endocrine disruptors. Most common human exposure to these compounds may occur with contaminated food. They may migrate into food from plastic wrap or may enter food from general environmental contamination. Since these substances are not limited to the original products, and enter the environment, they have become widespread environmental pollutants, thus leading to a variety of phthalates that possibly threaten the public health. To determine whether seven phthalate analogues i.e. diallyl phthalate, diisodecyl phthalate, di-n-nonyl phthalate, butyl benzyl phthalate, di-n-octyl phthalate, di-tridecyl phthalate, and dibutyl phthalate, can induce DNA strand breakage that is one of the various factors related to the mechanism of carcinogenicity, the comet assay which has been widely used for the detection and measurement of DNA strand breaks, was conducted in L5178Y mouse lymphoma cells. From these results, seven phthalates revealed dose-dependent decrease of cell viability, however, no remarkable cytotoxicity was observed even at high concentration of 100 $\mu\textrm{g}$/$m\ell$ phthalates. And also, the results showed that the induction of DNA strand breaks by seven phthalates was not significantly different from the control in this study.

• Environmental Analysis Health and Toxicology
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• v.16 no.1
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• pp.17-20
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• 2001

The alkaline comet assay, employing a single-cell gel electrophoresis(SCGE), is a rapid, simple and sensitive technique for visualizing and measuring DNA damage leading to strand breakage in individual mammalian cells. The protecting effect of pretreatment with vitamin C and cysteine on the DNA damage of gamma ray was investigated in mice splenic lymphocytes. Vitamin C and cysteine were administered orally for five consecutive days before irradiation. Four week old ICR male mice were irradiated wish 3.5Gy of γ-radiation and were sacrificed 3 days later. Spleens were taken for DNA damage examination by Comet assay and the tail moments of DNA single -strand breaks in tole splenic lymphocytes were evaluated. The results show that pretreatment with vitamin C and cysteine were effective in protecting against DNA damage by gamma ray. Administration of antioxidants like vitamin C and cysteine to mice before irradiation was effective in reducing the tail moment of splenic lymphocytes DNA.

• Environmental Mutagens and Carcinogens
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• v.7 no.2
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• pp.59-64
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• 1987

Cytotoxic and genotoxic potential of monosodium glutamate (MSG) were evaluated in primary cultures of rat hepatocytes. When exposed to liver cell culture continuously for 24 hr, MSG did not show any cytotoxic effects up to 0.5% (w/v) level as determined by Tryphan Blue exclusion and lactic dehydrogenase release test. MSG also did not induce unscheduled DNA synthesis or DNA single-strand breaks in hepatocyte cultures up to 1% level. No synergistic effects of MSG were observed on aflatoxin B$_1$-induced DNA damage when 1% MSG was treated to liver cell culture along with aflatoxin B$_1$.

• The Korean Journal of Zoology
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• v.26 no.3
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• pp.171-179
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• 1983

Amounts of DNA single strand breaks and unscheduled DNA synthesis in CHO cells exposed to MMS were increased in the presence of 3-aminobenzamide, a potent inhibitor of poly (ADP-ribose) polymerase. However, those in cells irradiated with UV-light were decreased. These results suggest that poly (ADP-ribose) polymerase acts negatively on the MMS-induced base excision repair but positively on the UV-induced nucleotide excision repair. In the combined treatment with MMS and UV-light in the presence of this inhibitor, amounts of strand breaks were just the same as those in the absence of the inhibitor. But those of unscheduled DNA synthesis were increased up to the amount induced by UV-light alone. These results may suggest that poly (ADP-ribose) polymerase affects the incision step of excision repair induced by MMS and UV-light independently, and that it may potentiate the complete cleaving of UV-induced pyrimidine dimers possibly by the repair enzymes which might have been partially inactivated by MMS.

• Environmental Mutagens and Carcinogens
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• v.15 no.2
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• pp.94-99
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• 1995

The adaptive response and cross-adaptive response to sister chromatid exchanges (SCEs) and DNA single-strand breaks (SSBs) in Chinese hamster ovary (CHO)-K$_1$ cells treated with ultraviolet radiation (UV), ethyl methanesuffonate (EMS), or bleomycin (BLM) were investigated. Two assays were used in this study; SCEs and alkaline elution. The pretreatment with low conditioning dose of 2 mM EMS or 1 J/m$^2$ UV decreased the yield of SCEs induced by subsequent treatment with 8 mM EMS, 5 J/m$^2$ UV or 5 $\mu$g/ml BLM. And the pretreatment with low conditioning dose of 1 $\mu$g/ml BLM decreased the yield of SCEs induced by subsequent treatment with 5 $\mu$g/ml BLM or 5 J/m$^2$ UV. The rejoining of DNA SSBs in cells subsequently treated with 2 J/m$^2$ UV, 50 mM EMS or 400 $\mu$g/ml BLM is higher than that only treated with 2 J/m$^2$ UV, 50 mM EMS or 400 $\mu$g/ml BLM. These results suggest that there are the adaptive response and cross-adaptive response to SCEs, and is the adaptive response to the rejoining of DNA SSBs in CHO cells.

• Journal of Photoscience
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• v.9 no.3
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• pp.49-50
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• 2002

N-Nitrosoproline(NPRO) is endogenously formed from proline and nitrite. NPRO has been reported to be nonmutagenic and noncarcinogenic. In this study, we have detected the direct mutagenicity of NPRO with UVA and UVB towards S. typhimurium. Formation of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), a mutagenic lesion, was observed in calf thymus DNA treated with NPRO plus simulated sunlight. Furthermore, the treatment with NPRO and sunlight induced single strand breaks in the superhelical replicative form of phage M13mp2 DNA. An analysis using scavengers suggested that both reactive oxygen species and NO radical mediate the strand breaks. The formation of nitric oxide was observed in NPRO solution irradiated with UVA. The co-mutagenic and co-toxic actions of NPRO and sunlight merit attention as possible mechanisms increasing the carcinogenic risk from UVA irradiation.

• Journal of Food Hygiene and Safety
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• v.31 no.1
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• pp.1-7
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• 2016

In the present study, our aim was to determine whether green tea extract (GTE) and its major constituent, epigallocatechin-3-gallate (EGCG) have a protective effect on ethanol-induced cytotoxicity and DNA damage in NIH/3T3 and HepG2 cells. The cell viability and DNA single strand breaks were examined by MTT assay and alkaline single cell gel electrophoresis (Comet assay), respectively. Ethanol decreased the cell viability and also increased DNA single strand breaks in a concentration-dependent manner. On the other hand, GTE showed the protective effect of cytotoxicity and DNA damage induced by ethanol in both cell lines. GTE and EGCG, were found to possess the anti-oxidative and anti-genotoxic activities by evaluation with DPPH test, LDL oxidation assay, oxidative DNA damage assay and 8OH-2'dG generation test. These results were also verified by the experimental results demonstrating the lower cytotoxicity and genotoxicity of commercial green tea liqueur compared to pure ethanol in same concentration. Thus it is concluded that the supplementation of GTE or EGCG may mitigate the ethanol-induced cytotoxicity and DNA damage.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1996.04a
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• pp.174-174
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• 1996

Extract of Pulsatilla Koreana (SB-31) showed promising antitumor activity in vitro (J. Kor Cancer Asso 26:959-963, 1994). We studied the mechanism of cytotoxicity of SB-31. HL-60 cells were cocultivated with various concentrations of SB-31 for 5 hours. The DNAs from HL-60 cells exposed to SB-31 showed the ladder pattern typical of apoptosis. Effect of SB-31 on topoisomerase I activity was determined by slight modification of the method by E. Aflalo(1994). The pBR322 DNA showed dose-dependent increase of R-Form DNA upon incubation with SB-31. The topoisomerase Ⅰ-like activity (Increase of R-Form DNA) was accentuated with higher dose of SB-31. It is postulated that SB-31, which is a fermentation product of Pulsatilla koreana and which loses its activity when kept in ambient temperature for more than 96 hours, may contain topoisomerase Ⅰ-like activity and the enhanced excessive single strand breaks induced by 55-31 may result in apoptosis.