• 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.

• Nutritional Sciences
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• v.7 no.3
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• pp.127-132
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• 2004

The current study examined the effects of mulberry fruit on the antioxidative defense systems and oxidative stress in the erythrocytes of diabetes-induced rats. Sprague-Dawley male rats were randomly assigned to one normal and three streptozotocin (STZ)-induced diabetic groups. 1be diabetic groups were fed a mulberry fruit-free diet (DM-group), 0.3% mulberry fruit diet (DM-F group) or 0.6% mulberry fruit diet (DM-2F group). Diabetes was induced with STZ after three weeks of the experimental diets. 1be rats were sacrificed 9 days later for examination of the antioxidative defense systems and oxidative stress in the erythrocytes. Means of cy-3-Ο-glucopyranoside, cy-3-Ο-rutinoside, rutin, isoquercitrin, quercetin, morin and dehydroquercetin contents were 230.45, 131.5, 142.5, 10.3, 5.8, 1.6 and 3.83mg per l00g dry weight, respectively, in the mulberry fruit. Mulberry fruit strengthened the antioxidative defense systems through increased activity of the antioxidant enzymes, such as glutathione peroxidase (GSH-px) and catalase (CAT), in the erythrocytes of the diabetes-induced rats. Accrdingly, mulberry fruit was found to reduce the accumulation of thiobarbituric acid reactive substance (WARS). Therefore, mulberry fruit was found to be excellent for strengthening the antioxidative defense system and reducing damaging oxidative substances in the erythrocytes of the diabetes-induced rats.

• Molecules and Cells
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• v.27 no.3
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• pp.279-282
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• 2009

"Two-cysteine" peroxiredoxins are antioxidant enzymes that exert a cytoprotective effect in many models of oxidative stress. However, under highly oxidizing conditions they can be inactivated through hyperoxidation of their peroxidatic active site cysteine residue. Sulfiredoxin can reverse this hyperoxidation, thus reactivating peroxiredoxins. Here we review recent investigations that have shed further light on sulfiredoxin's role and regulation. Studies have revealed sulfiredoxin to be a dynamically regulated gene whose transcription is induced by a variety of signals and stimuli. Sulfiredoxin expression is regulated by the transcription factor AP-1, which mediates its up-regulation by synaptic activity in neurons, resulting in protection against oxidative stress. Furthermore, sulfiredoxin has been identified as a new member of the family of genes regulated by Nuclear factor erythroid 2-related factor (Nrf2) via a conserved cis-acting antioxidant response element (ARE). As such, sulfiredoxin is likely to contribute to the net antioxidative effect of small molecule activators of Nrf2. As discussed here, the proximal AP-1 site of the sulfiredoxin promoter is embedded within the ARE, as is common with Nrf2 target genes. Other recent studies have shown that sulfiredoxin induction via Nrf2 may form an important part of the protective response to oxidative stress in the lung, preventing peroxiredoxin hyperoxidation and, in certain cases, subsequent degradation. We illustrate here that sulfiredoxin can be rapidly induced in vivo by administration of CDDO-TFEA, a synthetic triterpenoid inducer of endogenous Nrf2, which may offer a way of reversing peroxiredoxin hyperoxidation in vivo following chronic or acute oxidative stress.

• Journal of Ginseng Research
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• v.34 no.2
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• pp.138-144
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• 2010

Ginseng (Panax ginseng C.A. Meyer) has been shown to have anti-stress effects in animal studies. However, most studies have only managed to detect altered levels of biomarkers or enzymes in blood or tissue, and the actual molecular mechanisms by which ginseng exerts these effects remain unknown. In this study, the anti-oxidative effect of Korean red ginseng (KRG) was examined in human SK-N-SH neuroblastoma cells. Incubation of SK-N-SH cells with the oxidative stressor hydrogen peroxide resulted in significant induction of cell death. In contrast, pre-treatment of cells with KRG decreased cell death significantly. To elucidate underlying mechanisms by which KRG inhibited cell death, the expression of apoptosis-related proteins was examined by Western blot analysis. KRG pre-treatment decreased the expression of the pro-apoptotic gene caspase-3, whereas it increased expression of the anti-apoptotic gene Bcl-2. Consistent with this, immunoblot analysis showed that pre-treatment of the SK-N-SH cells with KRG inhibited expression of the pro-inflammatory gene cyclooxygenase 2 (COX-2). RT-PCR analysis revealed that the repression of COX-2 expression by KRG pre-treatment occurred at the mRNA level. Taken together, our data indicate that KRG can protect against oxidative stress-induced neuronal cell death by repressing genes that mediate apoptosis and inflammation.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.12
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• pp.5059-5062
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• 2015

Background: ALL is an irredeemable disease due to the resistance to treatment. There are several influences which are involved in such resistance to chemotherapy, including oxidative stress as a result of the generation of reactive oxygen species (ROS) and presence of hypodiploid cells. Cluster of differentiation 26 (CD26), also known as dipeptidyl peptidase-4, is a 110 kDa, multifunctional, membrane-bound glycoprotein. Aim and objectives: The aim of this study was to evaluate the clinical significance of serum CD26 in patients with acute lymphoblastic leukaemia patients in the post remission induction phase, as well as the relationship between CD26 activity and the oxidative stress status. Materials and Methods: CD26, total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI), in addition to activity of related enzymes myeloperoxidase, glutathione-s-transferase and xanthine oxidase, were analysed in sixty children with acute lymphoblastic leukaemia in the post remission induction phase. Results: The study showed significant elevation in CD26, TOS and OSI levels in patients with acute lymphoblastic leukaemia in the post remission induction phase in comparison to healthy control samples. In contrast, myeloperoxidase, glutathione-s-transferase and xanthine oxidase activities were decreased significantly. A significant correlation between CD26 concentration and some oxidative stress parameters was evident in ALL patients. Conclusions: Serum levels of CD26 appear to be useful as a new biomarker of oxidative stress in children with acute lymphoblastic leukaemia in the post remission induction phase, and levels of antioxidants must be regularly estimated during the treatment of children with ALL.

• Preventive Nutrition and Food Science
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• v.11 no.2
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• pp.94-99
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• 2006

This study investigated the protective effect of the butanol (BuOH) fraction from Laminaria japonica (BFLJ) extract on high glucose-induced oxidative stress in human umbilical vein endothelial cells (HUVECs). Freeze-dried L japonica was extracted with distilled water, and the extracted solution was mixed with ethanol then centrifuged. The supernatant was subjected to sequential fractionation with various solvents. The BuOH fraction was used in this study because it possessed the strongest antioxidant activity among the various solvent fractions. To determine the protective effect of the BFLJ, oxidative stress was induced by exposing of HUVECs to the high glucose (30 mM) or normal glucose (5.5 mM) for 48 hr. Cell viability, lipid peroxidation, glutathione (GSH) concentration, and antioxidant enzyme activities such as catalase, superoxide dismutase (SOD), glutathione peroxidase (GSH-px), and glutathion reductase (GSH-re) were measured. Exposure of HUVECs to high glucose for 48 hr resulted in a significant (p<0.05) decrease in cell viability, SOD, GSH-px and GSH-re and a significant (p<0.05) increase in thiobarbituric acid reactive substances (TBARS) formation in comparison to the cells treated with 5.5 mM glucose or untreated with glucose. BFLJ treatment decreased TBARS formation and increased cell viability, GSH concentration, and activities of antioxidant enzymes including catalase, SOD, GSH-px, and GSH-re in high glucose pretreated HUVECs. These results suggest that BFLJ may be able to protect HUVECs from high glucose-induced oxidative stress, partially through the antioxidative defence systems.

• Food Science and Biotechnology
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• v.16 no.2
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• pp.205-211
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• 2007

This study was designed to investigate the suppressive effect of chlorophyll a on nitric oxide (NO) production and intracellular oxidative stress. In addition, chlorophyll a regulation of nuclear factor (NF) ${\kappa}B$ activation and inducible NO synthase (iNOS) expression were explored as potential mechanisms of NO suppression in a lipopolysaccharide (LPS)-stimulated macrophage cell line. RAW 264.7 murine macrophages were preincubated with various concentrations ($0-10\;{\mu}g/ mL$) of chlorophyll a and stimulated with LPS to induce oxidative stress and inflammatory response. Treatment with chlorophyll a reduced the accumulation of thiobarbituric acid-reactive substances (TBARS), enhancing glutathione level and the activities of antioxidative enzymes including superoxide dismutase, catalase, glutathione peroxidase (GSH-px), and glutathione reductase in LPS-stimulated macrophages compared to LPS-only treated cells. NO production was significantly suppressed in a dose-dependent manner (p<0.05) with an $IC_{50}$ of $12.8\;{\mu}g/mL$. Treatment with chlorophyll a suppressed the levels of iNOS protein and its mRNA expression. The specific DNA binding activities of NFkB on nuclear extracts from chlorophyll a treated cells were significantly suppressed in a dose-dependent manner with an $IC_{50}$ of $10.7\;{\mu}g/mL$. Chlorophyll a ameliorates NO production and iNOS expression through the down-regulation of NFkB activity, which may be mediated by attenuated oxidative stress in RAW 264.7 macrophages.

• Journal of Ginseng Research
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• v.41 no.2
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• pp.159-168
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• 2017

Background: Radiotherapy is one of the most important modalities in cancer treatment; however, normal tissue damage is a serious concern. Drug development for the protection or reduction of normal tissue damage is therefore a clinical issue. Herein, we evaluated the protective properties of Panax ginseng Meyer and its corresponding mechanisms. Methods: C56BL/6 mice were orally pretreated with P. ginseng water extract (PGE; 25 mg/kg, 50 mg/kg, or 100 mg/kg) or intraperitoneally injected melatonin (20 mg/kg) for 4 d consecutively, then exposed to 15-Gy X-ray radiation 1 h after the last administration. After 10 d of irradiation, the biological properties of hematoxicity, fat accumulation, histopathology, oxidative stress, antioxidant activity, pro-inflammatory cytokines, and apoptosis signals were examined in the hepatic tissue. Results: The irradiation markedly induced myelosuppression as determined by hematological analysis of the peripheral blood. Steatohepatitis was induced by X-ray irradiations, whereas pretreatment with PGE significantly attenuated it. Oxidative stress was drastically increased, whereas antioxidant components were depleted by irradiation. Irradiation also notably increased serum liver enzymes and hepatic protein levels of pro-inflammatory cytokines. Those alterations were markedly normalized by pretreatment with PGE. The degree of irradiation-induced hepatic tissue apoptosis was also attenuated by pretreatment with PGE, which was evidenced by a terminal deoxynucleotidyl transferase 2'-deoxyuridine 5'-triphosphate nick-end labeling assay, western blotting, and gene expressions analysis, particularly of apoptotic molecules. Conclusion: We suggest that PGE could be applicable for use against radiation-induced liver injury, and its corresponding mechanisms involve the modulation of oxidative stress, inflammatory reactions, and apoptosis.

• Molecules and Cells
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• v.38 no.12
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• pp.1071-1078
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• 2015

Superovulation induced by exogenous gonadotropin treatment (PMSG/hCG) increases the number of available oocytes in humans and animals. However, Superovulatory PMSG/hCG treatment is known to affect maternal environment, and these effects may result from PMSG/hCG treatment-induced oxidative stress. 2-Cys peroxiredoxins (2-Cys Prxs) act as antioxidant enzymes that protect cells from oxidative stress induced by various exogenous stimuli. Therefore, the objective of this study was to test the hypothesis that repeated PMSG/hCG treatment induces 2-Cys Prx expression and overoxidation in the reproductive tracts of female mice. Immunohistochemistry and western blotting analyses further demonstrated that, after PMSG/hCG treatment, the protein expression levels of 2-Cys Prxs increased most significantly in the ovaries, while that of Prx1 was most affected by PMSG/hCG stimulation in all tissues of the female reproductive tract. Repeated PMSG/hCG treatment eventually leads to 2-Cys Prxs overoxidation in all reproductive organs of female mice, and the abundance of the 2-Cys Prxs-$SO_{2/3}$ proteins reported here supports the hypothesis that repeated superovulation induces strong oxidative stress and damage to the female reproductive tract. Our data suggest that excessive oxidative stress caused by repeated PMSG/hCG stimulation increases 2-Cys Prxs expression and overoxidation in the female reproductive organs. Intracellular 2-Cys Prx therefore plays an important role in maintaining the reproductive organ environment of female mice upon exogenous gonadotropin treatment.

• Journal of Ginseng Research
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• v.37 no.4
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• pp.442-450
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• 2013

The aim of this study was to determine and compare the preventive effect of Korean White Ginseng and Red Ginseng on oxidative stress in $H_2O_2$-treated HepG2 cells. The roots of ginseng were extracted with 70% methanol and partitioned with butanol to obtain saponin fractions, which have been known as bioactive constituents of ginseng. 2',7'-Dichlorofluorescein diacetate (DCF-DA) assay and malondialdehyde (MDA) content were measured for evaluating intracellular reactive oxygen species (ROS) generation. Also, mRNA expressions and activities of antioxidant enzymes were analyzed to determine the antioxidant activity of saponin or non-saponin fractions of ginsengs. According to DCF-DA assay, $H_2O_2$-induced MDA release and ROS generation were significantly reduced by treatment with saponin fractions of white and red ginseng roots. Also, saponin fractions increased effectively intracellular antioxidant enzyme activities including catalase, glutathione peroxidase and superoxide dismutase in $H_2O_2$-treated HepG2 hepatoma cells. In general, red ginseng was more effective than white ginseng for reducing oxidative stress. These results indicate that administration of red ginseng may certainly contribute relatively stronger than white ginseng to prevent from damaging liver function by oxidative stress.