• Journal of Nutrition and Health
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• v.40 no.8
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• pp.701-707
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• 2007

This study was to investigate lipid peroxidation, antioxidant enzyme activity and DNA damage after exercise, and the protective effect of garlic against exercise-induced oxidative stress. Male Sprague-Dawley rats(4 weeks old) were randomly divided into three groups of 6 rats each; control group(Con) without garlic and exercise, Ex group with exercise alone, and Ex-G group with 2% garlic and exercise. For 4 weeks, rats were given diets containing 15% corn oil and 1% cholesterol with or without garlic. The swimming was selected as a model for exercise performance. Rats swam for 40 min a day, for 5 days a week. Group Ex and Ex-G showed significant lowering in body weight gain and fat accumulation compared to control. No significant changes were observed in levels of plasma cholesterol and triglyceride among three groups, demonstrating that exercise and garlic had no effects on changes of blood lipid. This finding of blood lipid seems to be due to higher plant sterol content in corn oil. The DNA tail moment of lymphocytes showed greater tendency in Ex and Ex-G than in control, but garlic supplements failed to suppress DNA damages. Compared to control, Ex had higher plasma TBARS which was lowered to the control's level in Ex-G with 2% garlic supplementation(p<0.05). Ex-G led to a higher hepatic superoxide dismutase(SOD) activity than control and Ex(p<0.05). Activity of hepatic catalase was also increased in Ex-G, while in Ex it was significantly low(p<0.05). It seemed that TBARS levels were related to the activities of SOD and catalase, and that garlic contributed to increasing the enzyme activities and led to decrease of TBARS. These results demonstrate that lipid peroxidation and DNA damage occur as a consequences of oxidative stress after exercise, and that antioxidant defense against oxidative stress could be enhanced by garlic supplementation through the induction of antioxidant enzymes. However, further investigations should be done on the garlic effect on DNA damage.

• The Korean Journal of Food And Nutrition
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• v.28 no.1
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• pp.34-39
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• 2015

In this study, portective effect on DNA damage several mushrooms (Pleurotus ostreatus, Flammulina velutipes, Lentinula edodes) according to cooking methods was investigated using Comet assay. Three edible mushrooms were cooked by grilling, blanching, pan-frying, or by preparing 'Jeon' (traditional Korean pancake). Cells were incubated in medium with 4 kinds of samples for 48 h ($37^{\circ}C$) were further treated with hydrogen peroxide ($H_2O_2$) for 5 min as an oxidative stimulus. Oxidative damage was evaluated by single-cell gel electrophoresis (Comet assay) and quantified by tail DNA% (TD), tail length (TL), tail moment (TM). Though oxidative DNA damages expressed as TD, TL, TM of 4 cooked samples were higher than raw sample, which means lower protective activities, all samples including raw sample had significantly higher protective effects than the positive control (p<0.05). The protective effect on DNA damage of cooked samples decreased much more when soybean oil added, likely due to the thermal oxidation of oil during cooking. Although heat treatment could degrade protective effect on DNA damage of mushrooms, the cooked mushroom had significant effect on oxidative stress. In conclusion, grilling and blanching were the most advantageous cooking methods to protect oxidative DNA damage induced by $H_2O_2$.

• Journal of Sasang Constitutional Medicine
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• v.14 no.1
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• pp.79-89
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• 2002

To evaluate the effect of Yuldahansotang(YHT) water extract on cultured hippocampal cell was inhibited by hydrogen peroxide, MTT assay, NR assay, Neurofilament enzymeimmuno assay and DNA synthesis assay were carried out after the cultured hippocampal cells were preincubated with various concentrations of YHT water extract for 3 hours prior to exposure of hydrogen peroxide. The results obtained were as follows: 1. Hydrogen Peroxide decreased the survival rate of the cultured hippocampal cells on NR assay and MIT assay. 2. YHT water extract have efficacy of increasing a amount of neurofilament decreased by hydrogen peroxide in cultured hippocampal cells. 3. YHT water extract have efficacy of increasing DNA synthesis decreased by hydrogen peroxide in cultured hippocampal cells. From above the results, It is concluded that YHT has marked efficacy in preventing for the damages by hydrogen peroxide.

• Journal of the Korean Society of Food Science and Nutrition
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• v.36 no.10
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• pp.1271-1278
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• 2007

In this study, the ability of Styela clava or Styela plicata to reduce ethanol-induced hepatotoxicity and hepatic and leucocytic DNA damages was evaluated. Twenty four male SD rats were given 25% ethanol containing water (ad lib, p.o.) and divided into 3 groups; ethanol treated control group (EtOH), ethano1+3% S. clava (EtOH+SC), and ethano1+3% S. plicata (EtOH+SP). After 6 weeks, the supplementation of S. clava reduced the plasma ALT, ALP and LDH activities significantly (p<0.05), while S. plicata induced significant decrease in the plasma LDH activity only. The comet assay was employed to quantify the alcohol-induced DNA damage in rat hepatocytes and leucocytes. A significant protective effect on hepatic and leucocytic DNA damages was observed in S. clava or S. plicata supplemented groups compared to the EtOH control group. The hepatic DNA damage was correlated positively with plasma ALP and LDH activities. These results demonstrated that S. clava or S. plicata supplementation protected alcohol-induced hepatic and leucocytic DNA damage.

• Journal of the korean academy of Pediatric Dentistry
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• v.27 no.1
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• pp.77-84
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• 2000

Although ferric sulfate has been proposed as an alternative to formocresol in pulpotomy treatment in primary teeth, it has been given little concern regarding its cytotoxicity and mutagenicity. In the present study, we assessed the in vitro genotoxic effect of a ferric sulfate on human gingival fibroblast cell line (HGF-1). DNA damage was evaluated using comet assay (single cell alkaline gel electrophoresis) and obtained the results as follows: 1. A dose-response relationship was found between ferric sulfate concentrations (0 to 5mM) and DNA damages. 2. Above the concentration of 0.1mM, DNA damage was significantly increased than those of the control (p<0.05). 2. At the fixed concentration of 0.05mM, no significant difference was found between exposure time and DNA damage. These findings suggest that ferric sulfate as a pulpotomy agent can induce DNA damage in human gingival fibroblasts.

• Journal of Life Science
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• v.21 no.12
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• pp.1698-1704
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• 2011

In this study, we evaluated the protective effects of ethanol extracts from Dendranthema indicum on cell and DNA damages induced by oxidative stress. Antioxidant activities of D. indicum extracts are higher than scavenging activities of DPPH free radical and hydroxyl radical by 92.8% and 73.8%, respectively, and higher than ferrous iron chelating effects by 59.4%. D. indicum extracts showed a protective effect on oxidative cell damage by inhibiting lipid peroxidation by 90.3% in the control group, and inhibiting expression level of p21 protein by 79.6% for the control group. This means D. indicum extracts have a great protective effect against oxidative stress. DNA fragmentation inhibition in D. indicum extracts were 89.6% for the control group, which makes the movement of DNA tail reduced, and phosphorylation of H2AX was 20.2% of the radical experiment group. This means that D. indicum extracts effectively inhibit DNA fragmentation and H2AX phosphorylation. Taken together, we suggest that ethanol extract from D. indicum has a role as a useful chemopreventor against oxidative damage.

• Biomolecules & Therapeutics
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• v.24 no.6
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• pp.604-609
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• 2016

5-fluorouracil (5-FU) is a chemotherapeutic agent commonly used for treatment of solid tumors, including colorectal cancer. However, chemoresistance against 5-fluorouracil (5-FU) often limits its success for chemotherapy and, therefore, finding out appropriate adjuvant(s) that might overcome chemoresistance against 5-FU bears a significant importance. In the present study, we have found that ${\alpha}$-mangostin can sensitize 5-FU-resistant SNUC5/5-FUR colon cancer cells to apoptosis. Exposure of ${\alpha}$-mangostin induced significant DNA damages and increased the intracellular 8-hydroxyguanosine (8-OH-G) and 4-hydroxynonenal (4-HNE) levels in SNUC5 and SNUC5/5-FUR cells. Western blot analysis illustrated that ${\alpha}$-mangostin-induced apoptosis was mediated by the activation of the extrinsic and intrinsic pathways in SNUC5/5-FUR cells. In particular, we observed that Fas receptor (FasR) level was lower in SNUC5/5-FUR cells, compared with SNUC5 cells and that silencing FasR attenuated ${\alpha}$-mangostin-mediated apoptosis in SNUC5/5-FUR cells. Together, our study illustrates that ${\alpha}$-mangostin might be an efficient apoptosis sensitizer that can overcome chemoresistance against 5-FU by activating apoptosis pathway.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.53 no.1
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• pp.123-131
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• 2020

In this study, we investigated the protective effects of a Neutrase enzymatic hydrolysate derived from Korea pen shell Atrina pectinata (APN) against hydrogen peroxide (H₂O₂)-induced oxidative damage in hepatocytes. First, we confirmed that APN has antioxidant activities by scavenging 2,2-azino-bis (3-ethylbenzthiazoline)-6-sulfonic acid radical (ABTS⁺) and H₂O₂ and increasing oxygen radical absorbance capacity (ORAC) value. Also, the treatment of APN increased the cell viability by reducing the intracellular reactive oxygen species (ROS) production in H₂O₂-stimulated hepatocytes. In addition, APN decreased the sub-G₁ DNA contents and the apoptotic body formation increased by H₂O₂ stimulation. Moreover, APN modulated the protein expression of apoptosis related molecules (Bcl-2, Bax and p53) by suppressing the activation of nuclear factor NFkB and ERK/p38 signaling in H₂O₂-stimulated hepatocytes. Furthermore, APN led to the activation of Nrf2/HO-1signaling known as antioxidant systems. These results suggest APN protects hepatocytes against oxidative damages caused by H₂O₂ stimulation.

• Korean Journal of Medicinal Crop Science
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• v.20 no.6
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• pp.487-492
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• 2012

Damages of medicinal crops by thrips and identification of thrips species were investigated by periodic surveys on major medicinal crops, Platycodon grandiflorum, Schizandra chinensis, Codonopsis lanceolata, Lycium chinense, Bupleurum falcatum, Ledebouriella seseloides, Angelica gigas, Glycyrrhiza uralensis, Liriope platyphylla, Atractyloides sp., once or twice a month in Suwon, Eumseong, Jecheon, Pyeongchang, Chyungyang from May to October in 2012. Thrips and their damages were found at all of the medicinal crops investigated, mostly occurring at early growing stages of each medicinal crop and causing apical meristem region withered, thereby inhibiting the growth of plants. For species identification of thrips collected from each medicinal crops, DNA from each individual was extracted and ITS2 and COI regions were amplified by PCR. As a result, Frankliniella intonsa, Thrips tabaci, and Megalurothrips distalis have been identified as dominant species on medicinal crops in open field, whereas Frankliniella occidentalis was restricted to Lycium chinense in which protected cultivation. This study suggests that the occurrence of thrips species on medicinal crops seems to be affected by host specificity and environmental factors such as cultivation types.

• Journal of Photoscience
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• v.9 no.2
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• pp.229-232
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• 2002

There are two distinct UV-responsive signaling pathways in UV-irradiated mammalian cells, i.e., the DNA damage-dependent and -independent pathways. The former occurs in nucleus and results in growth arrest and apoptosis via post-translational modification of p53. The latter is initiated by oxidative stress and/or by damages in cell membrane or cytoplasm, which activate signaling cascade through intracellular molecules including mitogen activated protein kinases (MAPK). In normal human fibroblastic cells, all of MAPK family members, extracellular signal-related kinases (ERK), c-Jun N-terminal kinases (JNK) and p38, were rapidly phosphorylated following UV-irradiation. ERK phosphorylation was suppressed by an inhibitor of receptor tyrosine kinases (RTK). As ERK usually responds to mitogenic stimuli from RTK ligands, UV-induced ERK phosphorylation may be linked to the proliferation of survived cells. In contrast, phosphorylation of JNK and p38, as well as apoptosis, were modulated by the level of UV-generated oxidative stress Therefore, JNK and p38 may take part in oxidative stress-mediated apoptosis. Phosphorylation of p53 at Ser and Thr residues are essential for stabilization and activation of p53. Among several sites reported, we confirmed phosphorylation at Ser-15 and Ser-392 after UV-irradiation. Both of these were inhibited by a phosphoinositide 3-kinase inhibitor, presumably due to the shutdown of signals from DNA damage to p53. Phosphorylation at Ser-392 was also sensitive to an antioxidant and a p38 inhibitor, suggesting that Ser-392 of p53 is one of the possible points where DNA damage-dependent and -independent apoptic signals merge. Thus, MAPK pathway links UV-induced intracellular signals to the nuclear responses and modifies DNA damage-dependent cellular outcome, resulting in the determination of cell death.