• Journal of Nutrition and Health
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• v.35 no.3
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• pp.279-290
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• 2002

This study was performed to assess age-related changes in DNA damage and antioxidative capacity in 4, 8, 12, 16, 20, and 24 months old Sprague-Dawley male rats. The following were measured the degree of oxidative DNA damage as indicated by levels of 8-hydroxy-2'-deoxyguanosine (80HdG) in the kidney ; the peroxidized lipid concentrations in the plasma and the liver, as indicated by the levels of thiobarbituric acid reactive substances (TBARS); and the levels of antioxidant enzyme activities in the erythrocytes and the liver. Both body weight (BW) and epididymal fat pad (EFP) weight per BW increased with age until 16 months, then decreased slightly from 20 to 24 months. However, the weights of the liver, kidney and spleen per BW decreased with age. Concentrations of 8-OHdG in the kidney increased with age, only slightly front 4 to 16 months, and then markedly from 16 to 24 months. TBARS concentrations in the plasma and liver were shown to increase with age, being lowest in the 4 month-old group and highest in the 24 month-old group. Superoxide dismutase (SOD) activity in the erythrocytes increased with age Catalase activity in the erythrocytes increased from 4 to 16 months, then decreased from 20 to 24 months. Glutathione peroxidase (GSH-Px) activity in the erythrocytes showed no age-related change. Liver SOD activity decreased with age, particularly from 16 to 20 months, but catalase and GSH-Px activities in the liver showed no significant changes. These results showed that during the normal aging of SD rats, DNA damage in the kidney and TBARS concentrations in the plasma and liver increased with age, particularly after 16 months, and the imbalance of antioxidative enzyme activities in the erythrocytes accelerated with age.

• Biomolecules & Therapeutics
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• v.17 no.1
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• pp.92-97
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• 2009

As nanomaterials might enter into cells and have high reactivity with intracellular structures, it is necessary to assay possible genotoxic risk of them. One of these approaches, we investigated possible genotoxic potential of gold nanoparticle (AuNP) using L5178Y cells. Four different sizes of AuNP (4, 15, 100 or 200 nm) were synthesized and the sizes and structures of AuNP were analyzed using transmission electron microscopy (TEM), scanning electron microscopy (SEM) and stability was analyzed by a UV/Vis. Spectrophotometer. Cytotoxicity was assessed by direct cell counting, and cellular location was detected by dark field microscope at 6, 24 and 48 h after treatment of AuNP. Comet assay was conducted to examine DNA damage and tumor necrosis factor (TNF)-${\alpha}$ mRNA level was assay by real-time reverse transcription polymerase chain reaction. Synthetic AuNP (4, 50, 100 and 200 nm size) had constant characteristics and stability confirmed by TEM, SEM and spectrophotometer for 10 days, respectively. Dark field microscope revealed the location of AuNP in the cytoplasm at 6, 24 and 48 h. Treatment of 4 nm AuNP induced dose and time dependent cytotoxicity, while other sizes of AuNP did not. However, Comet assay represented that treatment of 100 nm and 200 nm AuNP significantly increased DNA damage compared to vehicle control (p <0.01). Treatment of 100 nm and 200 nm AuNP significantly increased TNF-${\alpha}$ mRNA expression compared to vehicle control (p<0.05, p<0.01, respectively). Taken together, AuNP induced DNA damage in L5178Y cell, associated with induction of oxidative stress.

• Journal of Marine Bioscience and Biotechnology
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• v.13 no.2
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• pp.86-93
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• 2021

A high salt diet contributes to kidney damage by causing hypoxia and oxidative stress. Recently, an increase in dietary salt has been reported to induce an inflammatory phenotype in immune cells, further contributing to kidney damage. However, studies on the exact mechanism and role of a high salt diet on the inflammatory response in the kidneys are still insufficient. In this study, a cisplatin-induced acute kidney injury model using C57BL/6 mice was used to analyze the effect of salt intake on kidney injury. Results showed that high salt administration aggravated kidney edema in mice induced by treatment with cisplatin. Moreover, the indicators of kidney and liver function impairment were significantly increased in the group cotreated with high salt compared with that treated with cisplatin alone. Furthermore, the exacerbation of kidney damage by high salt administration was also associated with a decrease in the number of cells in the immune regulatory system. Additionally, high salt administration further decreased renal perfusion functions along with increased cisplatin-induced damage to proximal tubules. This was accompanied by increased expression of T cell immunoglobulin, mucin domain 1 (a biomarker of kidney injury), and Bax (a pro-apoptotic factor). Moreover, cisplatin-induced expression of proinflammatory mediators and cytokines, including cyclooxygenase-2 and tumor necrosis factor-α in kidney tissue, was further increased by high salt intake. Therefore, these results indicate that the kidney's inflammatory response by high salt treatment can further promote kidney damage caused by various pathological factors.

• Journal of Life Science
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• v.28 no.6
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• pp.708-717
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• 2018

The antioxidant activity and protective effects of a hot water extract from the Stauntonia hexaphylla fruit (WESHF) were investigated in vitro and in vivo. The total polyphenol and flavonoid contents of WESHF were $16.13{\pm}0.27mg$ gallic acid equivalent/g and $4.7{\pm}0.80mg$ catechin equivalent/g, respectively. In addition, the DPPH radical-scavenging activity ($SC_{50}$) and the Oxygen Radical Absorbance capacity of WESHF were $63.62{\pm}4.10{\mu}g/ml$ and $90.63{\pm}5.29{\mu}M$ trolox equivalent/g, respectively. The hepatoprotective effect of WESHF against hydrogen peroxide-induced oxidative damage was investigated. $H_2O_2$-induced liver damage on HepG2 cells was prevented by $200{\mu}g/ml$ of WESHF. Furthermore, to investigate the protection mechanism of WESHF on hydrogen peroxide-induced cytotoxicity in HepG2 cells, pre-treatment with $200{\mu}g/ml$ of WESHF significantly attenuated a decrease in the activities of CAT, SOD, GR, and GPx. The hepatoprotective activity of WESHF was evaluated in an experimental model of hepatic damage induced by acetaminophen (APAP). The levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were significantly decreased in the livers of mice treated with 200 mg/kg of WESHF compared to the APAP-treated group. The lipid peroxidation level, which increased after APAP administration, was significantly reduced in the WESHF group. In addition, histological examinations of the liver showed the same protective effect of WESHF treatment. Based on these findings, it is suggested that WESHF has potent hepatoprotective effects, and the mechanism that causes this type of protection could be related to antioxidant pathways.

• Journal of the Korean Society of Food Science and Nutrition
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• v.32 no.2
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• pp.278-286
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• 2003

Alcohol is well known agent which can damage the human tissues such as liver via stimulating lipid peroxidation. On the other hand, carotenoids in addition to vitamins A, C and I play important roles in protecting these oxidative damages as well as preventing the production of free radicals. This study was carried out to investigate the effect of dietary vitamin A on lipid peroxidation and antioxidants status in ethanol-treated rats. In the experiment, male Sprague-Dawley rats weighing 160~180 g were given a liquid diet containing 36% of total calories as ethanol for 7 weeks. The pair-fed control rats received an isocaloric amount of diet containing sucrose instead of ethanol on the following day Additionally, the liquid diet contained adequate amount of $\beta$-carotene, retinyl acetate or 13-sis-reinoic acid except vitamin A-deficient diet. The results obtained are as follows. The levels of plasma and hepatic lipid peroxide were increased after chronic ethanol feeding in rats. Retinyl acetate supplementation significantly reduced lipid peroxidation induced by ethanol feeding Glucose 6-phosphatase activity was significantly reduced in rats fed vitamin A-deficient diet with ethanol and alkaline phosphatase activity was significantly induced in rats fed 13-cis-reinoic acid diet with ethanol. Catalase and alcohol dehydrogenase activities did not show a consistent tendency in experiment groups. The hepatic antioxidant enzyme activities did not significantly changed by chronic ethanol feeding groups. The striking decrease in conversion of $\beta$-carotene to retinol was observed in rats fed a $\beta$-carotene diet with ethanol feeding The level of retinol and retinoic acid in plasma and liver was decreased after chronic ethanol administration Based on this result, these data suggest that ethanol feeding enhances oxidative stress especially in those fed a vitamin A-deficient diet, and vitamin A supplementation, especially, retinyl acetate intake can prevent enhanced lipid peroxidation and related damage to some extent.

• Journal of Life Science
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• v.27 no.9
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• pp.1070-1077
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• 2017

Chondrocyte apoptosis induced by reactive oxygen species (ROS) plays an important role in the pathogenesis of osteoarthritis. Schisandrin A, a bioactive compound found in fruits of the Schisandra genus, has been reported to possess multiple pharmacological and therapeutic properties. Although several studies have described the antioxidant effects of analogues of schisandrin A, the underlying molecular mechanisms of this bioactive compound remain largely unresolved. The present study investigated the cytoprotective effect of schisandrin A against oxidative stress (hydrogen peroxide [$H_2O_2$]) in SW1353 human chondrocyte cells. The results showed that schisandrin A preconditioning significantly inhibited $H_2O_2-induced$ growth inhibition and apoptotic cell death by blocking the degradation of poly (ADP-ribose) polymerase proteins and down-regulating pro-caspase-3. These antiapoptotic effects of schisandrin A were associated with attenuation of mitochondrial dysfunction and normalization of expression changes of proapoptotic Bax and antiapoptotic Bcl-2 in $H_2O_2-stimulated$ SW1353 chondrocytes. Furthermore, schisandrin A effectively abrogated $H_2O_2-induced$ intracellular ROS accumulation and phosphorylation of histone H2AX at serine 139, a widely used marker of DNA damage. Thus, the present study demonstrates that schisandrin A provides protection against $H_2O_2-induced$ apoptosis and DNA damage in SW1353 chondrocytes, possibly by prevention of ROS generation. Collectively, our data indicate that schisandrin A has therapeutic potential in the treatment of oxidative disorders caused by overproduction of ROS.

• Microbiology and Biotechnology Letters
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• v.46 no.1
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• pp.18-28
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• 2018

In this study, the antioxidant activities and cytoprotective effects against oxidative stress of Lonicera japonica Thunb. 50% ethanol extract and ethyl acetate fraction were investigated. Using the 1,1-diphenyl-2-picrylhydrazyl assay, the free radical scavenging activity (FSC50) of L. japonica Thunb. 50% ethanol extract and ethyl acetate fraction was determined as 152.00 and $77.25{\mu}g/ml$, respectively. To measure the reactive oxygen species (ROS) scavenging activity, the total antioxidant capacity (OSC50) was determined by using a luminol-dependent chemiluminescence assay. The antioxidant activity of the ethyl acetate fraction ($0.33{\mu}g/ml$) was approximately four times stronger than that of the 50% ethanol extract ($1.12{\mu}g/ml$). The protective effect against $^1O_2$-induced cellular damage of human erythrocytes (${\tau}_{50}$) was 46.0 min at $10{\mu}g/ml$ of the 50% ethanol extract and 52.3 min at $1{\mu}g/ml$ of the ethyl acetate fraction. We also investigated the cytoprotective effects against oxidative stress induced by $H_2O_2$ and the intracellular ROS scavenging activity in response to UVB irradiation and found that the extract and fraction protected human skin cells from damage and reduced ROS. These results confirmed that L. japonica Thunb. was a valuable plant-derived natural antioxidant with potential for development as an antioxidative functional ingredient.

• Journal of Life Science
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• v.28 no.4
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• pp.454-464
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• 2018

Black soybeans are used as food sources as well as for traditional medicines because they contain an abundance of natural phenolic compounds. In this study, total phenolic contents (TPCs) of Korean black seed coat soybean varieties Socheongja (SCJ), Socheong 2 (SC2) and Cheongja 2 (CJ2) as well as their antioxidant capacities were investigated. Among them, TPCs were abundantly present in the order of CJ2$H_2O_2$-stimulated HaCaT human keratinocytes. Our results revealed that treatment with SCJ and SC2 prior to $H_2O_2$ exposure significantly increases the viability of HaCaT cells, indicating that the exposure of HaCaT cells to SCJ and SC2 conferred a protective effect against oxidative stress. SCJ and SC2 also effectively inhibited $H_2O_2$-induced apoptotic cell death through the blocking of mitochondrial dysfunction. SCJ and SC2 also attenuated the phosphorylation of Histone H2AX. Furthermore, they effectively induced the levels of thioredoxin reductase (TrxR) 1, a potent antioxidant enzyme, which is associated with the induction of nuclear transcription factor erythroid-2-like factor 2 (Nrf2); however, the protective effects of SCJ and SC2 were significantly reversed by Auranofin, a TrxR inhibitor. These results indicate that they have protective activity through the blocking of cellular damage related to oxidative stress via the Nrf2 signaling pathway. In conclusion, our study indicated that SCJ and SC2 might potentially serve as novel agents for the treatment and prevention of skin disorders caused by oxidative stress.

• Journal of the Korean Society of Food Science and Nutrition
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• v.39 no.8
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• pp.1179-1186
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• 2010

The antiradical property of hot water extract from dried radish (DR) or dried radish roasted with pressure (DRRP) was investigated in vitro and in LLC-PK1 cell system. The contents of total free amino acid and reducing sugar in DR were decreased by 72.86% and 3.17%, respectively, after pressurized roasting. In vitro test, $IC_{50}$ for DR and DRRP for DPPH radical scavenging activity were 646.70 and $135.45\;{\mu}g/mL$, 896.10 and $566.98\;{\mu}g/mL$ for superoxide anion radical, and 722.26 and $531.84\;{\mu}g/mL$ for hydroxy radical, respectively. The radical scavenging effects of DRRP was significantly greater than those for DR (p<0.001). These radical scavenging effects of DR and DRRP were confirmed in LLC-$PK_1$ at which oxidative stresses were induced by superoxide, nitric oxide and peroxynitrite generated in the treatment of pyrogallol, SNP, and SIN-1, respectively. Cell viability was increased in the presence of DR or DRRP, dose dependently (p<0.05), and TBARS formation was decreased. The protective effects of DRRP against oxidative damage in LLC-$PK_1$ were greater than those of DR at the same concentration tested (p<0.05). This superior antiradical activity of DRRP might be due to the products produced during the pressurized roasting in addition to the antioxidative compounds originally present in the radish. 5-hydroxyl methyl furfural (5-HMF) known as an intermediate product of the maillard reaction was detected in DRRP (0.57 mg/g), but not from DR. In conclusion, daily consumption of DRRP may prevent oxidative damage by retarding oxidative stress.

• Journal of the Korean Society of Food Science and Nutrition
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• v.38 no.6
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• pp.683-693
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• 2009

This study was designed to investigate the effect of dandelion juice supplementation on attenuation of oxidative stress and hangover after drinking alcohol in healthy college male students. This human trial was conducted by two phase cross over design with two weeks wash out period. The subjects (age $24{\sim}28$ years) were volunteers who had more than 72 g of ethanol drinking capacity. Dandelion group was given dandelion juice 220 mL daily for 7 days. Biochemical markers were determined in blood samples taken at 0 and 150 minutes after administration 72 g of alcohol. The levels of plasma glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, lactate dehydrogenase and bilirubin, the indicators of liver cell damage, were not significantly different between groups. No significant differences in lymphocyte DNA damage level between groups was observed. However, plasma acetaldehyde dehydrogenase (ALDH) and high density lipoprotein cholesterol levels were significantly (p<0.01) increased in dandelion supplemented group compared to that of control group. Furthermore, activities and protein expressions of glutathione-reductase and catalase of erythrocytes were significantly elevated in dandelion supplemented group compared to that of control group. From the above results, it is concluded that dandelion juice supplementation can reduce oxidative stress and hangover syndrome through the elevation of ALDH and antioxidative enzyme system in healthy male adults.