• 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 Toxicology Conference
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• 2006.11a
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• pp.55-64
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• 2006

The fetal central nervous system (CNS) is sensitive to diverse environmental factors, such as alcohol, heavy metals, irradiation, mycotoxins, neurotransmitters, and DNA damage, because a large number of processes occur during an extended period of development. Fetal neural damage is an important issue affecting the completion of normal CNS development. As many concepts about the brain development have been recently revealed, it is necessary to compare the mechanism of developmental abnormalities induced by extrinsic factors with the normal brain development. To clarify the mechanism of fetal CNS damage, we used one experimental model in which 5-azacytidine (5AZC), a DNA damaging and demethylating agent, was injected to the dams of rodents to damage the fetal brain. 5AzC induced cell death (apoptosis)and cell cycle arrest in the fetal brain, and it lead to microencephaly in the neonatal brain. We investigated the mechanism of apoptosis and cell cycle arrest in the neural progenitor cells in detail, and demonstrated that various cell cycle regulators were changed in response to DNA damage. p53, the guardian of genome, played a main role in these processes. Further, using DNA microarray analysis, tile signal cascades of cell cycle regulation were clearly shown. Our results indicate that neural progenitor cells have the potential to repair the DNA damages via cell cyclearrest and to exclude highly affected cells through the apoptotic process. If the stimulus and subsequent DNA damage are high, brain development proceeds abnormally and results in malformation in the neonatal brain. Although the mechanisms of fetal brain injury and features of brain malformation afterbirth have been well studied, the process between those stages is largely unknown. We hypothesized that the fetal CNS has the ability to repair itself post-injuring, and investigated the repair process after 5AZC-induced damage. Wefound that the damages were repaired by 60 h after the treatment and developmental processes continued. During the repair process, amoeboid microglial cells infiltrated in the brain tissue, some of which ingested apoptotic cells. The expressions of genes categorized to glial cells, inflammation, extracellular matrix, glycolysis, and neurogenesis were upregulated in the DNA microarray analysis. We show here that the developing brain has a capacity to repair the damage induced by the extrinsic stresses, including changing the expression of numerous genes and the induction of microglia to aid the repair process.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.48 no.1
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• pp.33-38
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• 2022

Ultraviolet B (UVB) damages DNA residues in skin keratinocytes. In particular, the formation of cyclobutane pyrimidine dimers (CPD), a pyrimidine residue damage in DNA, is considered a representative indicator of skin photoaging. In this study, we confirmed defensive effect of Glycyrrhiza glabra (G. glabra) extract against UVB induced DNA damage. First of all, we confirmed UVB dependent amount of CPD formation in human keratinocyte cell line. UVB induced CPD was decreased by G. glabra extract by dose dependent manner. In addition, it was confirmed that the expression of mRNA of DNA damage recovery factors was increased by G. glabra extract. Consequently, through this study, it was possible to confirm the DNA protection effect of G. glabra extract in skin keratinocytes.

• Proceedings of the Korea Society of Environmental Biology Conference
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• 2003.11a
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• pp.68-73
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• 2003

The possibility of using the alkaline protocol of the single cell gel electrophoresis (SCGE) assay as a method for detecting induced DNA damage has been studied for six major plants. The EMS was applied as a model genotoxic agent on young excised leaves of the tested crops for 18 h at 26$^{\circ}C$ in the dark. With increasing concentrations of 0 to 10 mM EMS, the DNA damage, expressed by the averaged median tail moment values, significantly increased in nuclei of all plants studied. As the results, no correlation between the diameter of nuclei and sensitivity to EMS treatment was observed. The data obtained demonstrate the feasibility of using the SCGE assay for detecting induced DNA damage in plants.

• Journal of Life Science
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• v.14 no.3
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• pp.406-410
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• 2004

Glyoxal or methylglyoxal was incubated with catalase in 0.24 M sodium phosphate buffer (pH 7.4) at 37$^{\circ}C$. Dicarbonyls modify and inactivate catalase. Plasmid DNA that is directly incubated with glycation propagators, glyoxal and methylglyoxal, showed different DNA mobility shift compared to nomal plasmid DNA. When plasmid DNA is added in Fenton reaction with glycated catalase, plasmid DNA was significantly strand broken and 8-hydroxydeoxyguanosine production was time dependently increased. These results suggest that glycation of antioxidant is synergistic effect to oxidative stress.

• Korean Journal of Microbiology
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• v.38 no.2
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• pp.96-102
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• 2002

The S-phase checkpoint mechanisms response to DNA damage or inhibition of DNA replication for maintenance of genetic stability in eukaryotic cells. These roles include cell cycle control arrest at S-phase and Iranscriptional induction of repair genes. To characterize the defects of dpbll mutant for both these responses, we examined the over-expression effect of DPBll gene, the sensitivity to HU, MMS, and the transcriptional pattern by DNA damage agent for RNRS mRNA. RNRS transcript is induced in response to a wide variety of agents that either damage D7A directly through chemical modification or induce stress by blocking DNA synthesis. As results, dpbll-1 cells are sensitive to DNA damage agents and the level of RNR3 mRNA is reduced approximately 40% than wild type cells. Moreover, we found the same results in dpb2-1 cells. Therefore, we propose that DPB2 and DPBll act as a sensor of replication that coordinates the transcriptional and cell cycle responses to replication blocks.

• Natural Product Sciences
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• v.20 no.4
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• pp.237-242
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• 2014

Plant extracts produced from branches of Crataegus pinnatifida and barks of Crataegus pinnatifida inhibited ethanol-induced cytotoxicity and DNA damage in liver cells. Furthermore, these two extracts inhibited the expression and activities of CYP2E1 enzyme. Cinnamomum cassia had a better effect on inhibition of DNA damage than Crataegus pinnatifida, as well as showed a high tendency to inhibit CYP2E1 expression and catalytic activities. It is considered that extracts produced from Crataegus pinnatifida or Cinnamomum cassia have an effect to reduce ethanol-induced cytotoxicity and DNA damage in liver cells. Therefore, we suggest to use Crataegus pinnatifida and Cinnamomum cassia and their ingredients as potential candidate substances to prevent and treat ethanol-induced cytotoxicity and genotoxicity in liver cells.

• Korean Journal of Food Science and Technology
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• v.19 no.4
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• pp.311-316
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• 1987

The present paper was carried out to investigate the effects of active oxygen radicals on the DNA damage by linoleic acid peroxidation by using active oxygen scavengers in a linoleic acid-DNA system. DNA was greatly damaged by linoleic acid peroxidation, and the DNA damage was inhibited by the addition of active oxygen scavengers. Among active oxygen scavengers tested, ${\alpha}-tocopherol$ and superoxide dismutase greatly inhibited the DNA damage, but catalase and tris (hydroxymethyl) aminomethane didn't show such effects. Accordingly, singlet oxygen and superoxide anion greatly affected to the DNA damage occurring during linoleic acid peroxidation, and hydrogen peroxide was shown to participate in DNA damage in the early stage of peroxidation. And, the DNA damage by active oxygen radicals was mainly induced in the early stage of linoleic acid peroxidation.

• Journal of Food Hygiene and Safety
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• v.12 no.4
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• pp.315-320
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• 1997

Panax ginseng C.A. Meyer has been extensively used in the traditional oriental medicine as a restorative, tonic and prophylatic agent. This study was devised to develop a chemopreventive agent from panax ginseng to be able to suppress the genotoxicity and oxidative damage by ractive oxygen species, which are involved with cancer or aging. Ginseng petroleum ether extract (GPE) and one of its fraction, P2, showed an antioxidative effect on the lipid peroxidiphenyl-2-picryl hydrazil (DppH) radical generation. They also showed the suppressive effect of H2O2 or KO2 induced DNA damage by single cell gel electrophoresis (SCGE). Results from our study indicate that GPE and P2 are capable of protecting lipid peroxidation, and oxidative DNA damage. Therefore, GPE and P2 may be useful chempreventive agents which are involved with cancer and aging.

• Journal of Nutrition and Health
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• v.36 no.2
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• pp.125-132
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• 2003

The present study was attempted to investigate and compare the antioxidant potency of several well-know flavonoids, antioxidant vitamin and commercially available popular beverages. The antioxidant potency was assessed by the effect on reducing oxidative DNA damage of human lymphocytes. Cellular oxidative DNA damage was measured by SCGE (single-cell gel electrophoresis), also known as comet assay. Lymphocytes were pre-treated for 30 minutes with wide ranges of doses of apigenin, kaempferol, luteolin, myricetin, rutin, quercetin, $\alpha$-tocopherol (10,25,50,100,200,500,1000 $\mu$M) ,green tea extract or grape juice (10,50,100,250,500,1000 $\mu$g/mL) followed by a $H_2O$$_2$(100 $\mu$M) treatment for 5 min as an oxidative stimulus. The physiological function of each antioxidant substance on oxidative DNA damage was analyzed as tail moment (tail length $\times$ percentage migrated DNA in tail) and expressed as relative DNA damage score after adjusting by the level of control treatment. Cells treated with $H_2O$$_2$alone (positive control) had an extensive DNA damage compared with cells treated with phosphate buffered saline (PBS, negative control) or pre-treated with all the tested samples. Of all the six flavonoids, quercetin was the most potent antioxidant showing the lowest $ED_{50}$/ of 8.5 $\mu$g/mL (concentration to produce 50% protection of relative DNA damage). The antoxidant potency of individual flavonoids were ranked as follows in a decreasing order; luteolin (18.4 $\mu$g/mL), myricetin (19.0 $\mu$g/mL) , rutin (22.2 $\mu$g/mL) , apigenin (24,3 $\mu$g/mL) , kaempferol (25.5 $\mu$g/mL). The protective effect of $\alpha$-tocopherol was substantially lower (highest $ED_{50}$value of 55.0 $\mu$g/mL) than all the other flavonoids, while the protective effect was highest in green tea and grape juice with low ED5O value of 7.6 and 5.3, respectively. These results suggest that flavonoids, especially quercetin, and natural compounds from food product, green tea and grape juice, produced powerful anti-oxidative activities, even stronger than $\alpha$-tocopherol. Taken together, supplementation of antioxidants to lymphocytes followed by oxidative stimulus inhibited damage to cellular DNA, supporting a protective effect against oxidative damage induced by reactive oxygen species.