• Journal of Nutrition and Health
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• v.44 no.1
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• pp.5-15
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• 2011

Although iron is an essential mineral, excess iron intake during pregnancy may increase oxidative stress in tissues. This study was conducted to investigate the effects of iron overload during pregnancy on iron status and oxidative stress in maternal rats. Ten week-old female Sprague-Dawley rats were mated with male rats. Non-pregnant (control) and pregnant rats were fed diets containing normal Fe (35 mg/kg diet), high Fe (350 mg/kg diet), or excess Fe (1,050 mg/kg diet) during pregnancy. Rats were sacrificed on pregnancy day 19. No significant difference in weight gain, diet intake, or litter size was observed according to iron intake levels. Furthermore, serum iron, hemoglobin, and hematocrit were not different among the rats administered the three levels of Fe both in the control and pregnant groups. However, the iron levels were lower in pregnant rats than those in the control. The liver and spleen iron contents increased significantly in the excess Fe group. An increase in liver ferritin levels with increasing iron intake was observed. Protein carbonyl content, as a marker of oxidative stress, increased significantly in liver with increasing iron intake but not malondialdehyde. Glutathione peroxidase activity in the liver of pregnant rats fed excess iron decreased significantly. Bcl-2 protein expression in the liver declined remarkably with increasing maternal iron intake in pregnant rats. Taken together, iron overload during pregnancy had little effect on hematology. However, the deposits of iron in the liver and the decline in antioxidant enzyme activity implied increased oxidative stress in tissues of the excess Fe group. These results suggest that excess iron intake during pregnancy increases oxidative stress in maternal tissues and may also affect fetal tissues.

• Nutrition Research and Practice
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• v.11 no.3
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• pp.214-222
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• 2017

BACKGROUND/OBJECTIVES: Glutathione S-transferase (GST) forms a multigene family of phase II detoxification enzymes which are involved in the detoxification of xenobiotics by conjugating substances with glutathione. The aim of this study is to assess the antioxidative status and the degree of DNA damage in the subclinical hypertensive patients in Korea using glutathione S-transferase polymorphisms. SUBJECTS/METHODS: We examined whether DNA damage and antioxidative status show a difference between GSTM1 or GSTT1 genotype in 227 newly diagnosed, untreated (systolic blood pressure $(BP){\geq}130mmHg$ or diastolic $BP{\geq}85mmHg$) subclinical hypertensive patients and 130 normotensive subjects (systolic BP < 120 mmHg and diastolic BP < 80 mmHg). From the blood of the subjects, the degree of the DNA damage in lymphocyte, the activities of erythrocyte superoxide dismutase, the catalase, and the glutathione peroxidase, the level of glutathione, plasma total radical-trapping antioxidant potential (TRAP), anti-oxidative vitamins, as well as plasma lipid profiles and conjugated diene (CD) were analyzed. RESULTS: Of the 227 subjects studied, 68.3% were GSTM1 null genotype and 66.5% were GSTT1 null genotype. GSTM1 null genotype had an increased risk of hypertension (OR: 2.104, CI: 1.38-3.35), but no significant association in GSTT1 null genotype (OR 0.982, CI: 0.62-1.55). No difference in erythrocyte activities of superoxide dismutase, catalase, or glutathione peroxidase, and plasma TRAP, CD, lipid profiles, and GSH levels were observed between GSTM1 or GSTT1 genotype. Plasma levels of ${\alpha}-tocopherol$ increased significantly in GSTT1 wild genotype (P < 0.05); however, plasma level of ${\beta}-carotene$ increased significantly in GSTT1 null genotype (P < 0.01). DNA damage assessed by the Comet assay was significantly higher in GSTM1 null genotype than wild genotype (P < 0.05). CONCLUSIONS: These results confirm the association between GSTM1 null genotype and risk of hypertension as they suggest that GSTM1 null genotype leads to an increased oxidative stress compared with wild genotype.

• Journal of Environmental Science International
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• v.21 no.3
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• pp.267-276
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• 2012

Spaceflights results in the reduction of immune status of human beings and increase in the virulence of microorganisms, especially gram negative bacteria. The growth of Klebsiella pneumoniae is enhanced by catecholamines and during spaceflight, elevation in the levels of cortisols occurs. So it is necessary to know the changes in physiology, virulence, antibiotic resistance and gene expression of K. pneumoniae under microgravity conditions. The present study was undertaken to study effect of simulated microgravity on growth, morphology, antibiotic resistance and cross stress resistance of K. pneumoniae to various stresses. The susceptibility of simulated microgravity grown K. pneumoniae to ampicillin, penicillin, streptomycin, kanamycin, hygromycin and rifampicin were evaluated. The growth of bacteria was found to be fast compared with normal gravity grown bacteria and no significant changes in the antibiotic resistance were found. The bacteria cultured under microgravity conferred cross stress resistance to acid, temperature and osmotic stress higher than the normal gravity cultured bacteria but the vice versa was found in case of oxidative stress.

• Journal of Preventive Medicine and Public Health
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• v.36 no.4
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• pp.314-322
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• 2003

Objectives : In this study, the exposure status of the hazardous substances from incinerators, such as polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs), were studied , and the relationship between the exposure of these hazardous substances and their heath effects on the workers and residents near municipal solid waste (MSW) incinerators and an industrial incinerator investigated. Methods : Between July 2001 and Jure 2002, 13 workers at two MSW incinerators, 16 residents from the area around the two MSW incinerators, 6 residents from the control area, and further 10 residents near an industrial incinerator, estimated to emit higher levels of hazardous substances, were interviewed. Information, including sociodemographic information, personal habits, and work history, detailed gynecologic and other medical history were collected through interviews. Blood samples were also collected from 45 subjects, and analyzed for PCDD/DFs, by high resolution gas chromatography -high resolution mass spectrometry, using the US EPA 1613 method. In addition to the questionnaire survey, urinary concentrations of 8-hydroxydeoxyguanosine (8-OH-dG) and malondialdehyde (MDA) were measured as oxidative injury biomarkers. The urinary concentrations of 8-OH-dG were determined by in vitro ELISA, and the MDA by HPLC, using u adduct with thiobarbituric acid. Results : The PCDD/DFs concentrations in the residents near the industrial incinerator were higher than those in the controls, workers and residents near the MSW incinerators. The average TEQ (Toxic Equivalencies) concentrations of the PCDD/DFs in residents near the industrial incinerator were 53.4pg I-TEQs/g lipid. The estimated daily intakes were within the tolerable daily intake range (1-4 pg I-TEQ/Kg bw/day) suggested by WHO (1997) in only 30% to the people near the industrial incinerator. Animal studies have already shown that even a low body border of PCDD/DFs, such as 10 ng TEQ/kg bw, can cause oxidative damage in laboratory animals. Our study also showed that the same body burden of PCDD/DFs can cause oxidative damage to humans. Conclusions : The exposures to PCDD/DFs and the oxidative stress of residents near the industrial incinerator, were higher than those in the controls, workers and residents near the MSW incinerators. Proper protection strategies against these hazardous chemicals are needed. Because a lower body burden of PCDD/Fs, such as 10ng TEQ/kg bw, can cause oxidative damage, the tolerable daily intake range should be restrictedly limited to 1pg I-TEQ/kg bw/day.

• Asian-Australasian Journal of Animal Sciences
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• v.27 no.6
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• pp.907-915
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• 2014

Alpha-lipoic acid (${\alpha}$-LA) is not only involved in energy metabolism, but is also a powerful antioxidant that can protect against hepatic oxidative stress induced by some drugs, toxins, or under various physiological and pathophysiological conditions. Here, we investigated the effect of ${\alpha}$-LA against liver oxidative damage in broilers exposed to aflatoxin $B_1$ ($AFB_1$). Birds were randomly divided into four groups and assigned different diets: basal diet, 300 mg/kg ${\alpha}$-LA supplementation in basal diet, diet containing 74 ${\mu}g/kg$ $AFB_1$, and 300 mg/kg ${\alpha}$-LA supplementation in diet containing 74 ${\mu}g/kg$ $AFB_1$, for 3 weeks. The results revealed that the addition of 300 mg/kg ${\alpha}$-LA protected against the liver function damage of broilers induced by chronic low dose of $AFB_1$ as estimated by a significant (p<0.05) change in levels of plasma total protein, albumin, alkaline phosphatase and the activities of liver glutamic-oxalacetic transaminase and glutamic-pyruvic transaminase. The histopathological analysis also showed that liver tissues were injured in the $AFB_1$ diet, but this effect was alleviated by the addition of 300 mg/kg ${\alpha}$-LA. Additionally, $AFB_1$ induced a profound elevation of oxidative stress in birds, as indicated by an increase in malondialdehyde level, a decrease in glutathione peroxidase activity and a depletion of the glutathione content in the liver. All of these negative effects were inhibited by treatment with ${\alpha}$-LA. Our results suggest that the inhibition of $AFB_1$-induced excess production of lipid peroxides and the maintenance of intracellular antioxidant status may play important roles in the protective effects of ${\alpha}$-LA against $AFB_1$-induced oxidative damage in the liver.

• Journal of the Korean Society of Food Science and Nutrition
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• v.28 no.1
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• pp.257-264
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• 1999

This study was undertaken to investigate the relationship between the life style and the nutritional status of serum antioxidant vitamins and lipids in university male and female students. 48 male and 49 female students attending Andong university, aged between 18 and 25 years, were selected. Questions about the life styles including dietary intakes, food habits, smoking, drinking alcohol, exercise, stress were answered. And serum levels of antioxidant vitamins and lipids were determined. Average serum levels of total cholesterol, LDL C, HDL C, and triglyceride in male and female subjects were 158.6$\pm$32.7, 177.3$\pm$33.8; 86.4$\pm$26.0, 109.0$\pm$31.2; 46.0$\pm$10.7, 49.9$\pm$12.4; 131.2$\pm$22.5, 91.7$\pm$ 38.6mg/dl respectively. Average serum levels of antioxidant vitamin A, E and C in male and female subjects were 42.6$\pm$12.3, 31.4$\pm$9.8 g/dl, 1.11$\pm$0.38, 1.15$\pm$0.29mg/dl and 164.66 $\pm$65.01, 220.06$\pm$80.11 g/dl respectively. There was no significant difference between smoking habits and either serum lipids or antioxidant vitamins level. The serum vitamin C level of drinkers was significantly lower(p=0.038), but serum lipids(total cholesterol, LDL C, and triglyceride) were higher than non alcoholic subjects. The subjects with severe stress had lower in HDL C and higher in atherogenic index than others. This result indicates that oxidative stress may be increased in stressful environment from undesirable life styles and influence the status of serum lipid and antioxidant vitamins.

• Advances in Traditional Medicine
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• v.10 no.4
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• pp.239-253
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• 2010

Coenzyme $Q_{10}$ ($CoQ_{10}$, or ubiquinone) is an electron carrier of the mitochondrial respiratory chain (electron transport chain) with antioxidant properties. In view of the involvement of $CoQ_{10}$ in oxidative phosphorylation and cellular antioxidant protection a deficiency in this quinone would be expected to contribute to disease pathophysiology by causing a failure in energy metabolism and antioxidant status. Indeed, a deficit in $CoQ_{10}$ status has been determined in a number of neuromuscular and neurodegenerative disorders. Primary disorders of $CoQ_{10}$ biosynthesis are potentially treatable conditions and therefore a high degree of clinical awareness about this condition is essential. A secondary loss of $CoQ_{10}$ status following HMG-CoA reductase inhibitor (statins) treatment has been implicated in the pathophysiology of the myotoxicity associated with this pharmacotherapy. $CoQ_{10}$ and its analogue, idebenone, have been widely used in the treatment of neurodegenerative and neuromuscular disorders. These compounds could potentially play a role in the treatment of mitochondrial disorders, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, Friedreich's ataxia, and other conditions which have been linked to mitochondrial dysfunction. This article reviews the physiological roles of $CoQ_{10}$, as well as the rationale and the role in clinical practice of $CoQ_{10}$ supplementation in different neurological diseases, from primary $CoQ_{10}$ deficiency to neurodegenerative disorders. These will help in future for treatment of patients suffering from neurodegenerative disease.

• Asian-Australasian Journal of Animal Sciences
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• v.29 no.5
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• pp.681-688
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• 2016

The present study was conducted to compare the supplementation of natural (D-${\alpha}$-tocopherol) and synthetic (DL-${\alpha}$-tocopherol acetate) vitamin E on the growth performance, meat quality, muscular antioxidant capacity and genes expression related to oxidative status of broilers. A total of 144 1 day-old Arbor Acres broiler chicks were randomly allocated into 3 groups with 6 replicates of 8 birds each. Birds were given a basal diet (control group), and basal diet supplemented with either 20 IU D-${\alpha}$-tocopherol or DL-${\alpha}$-tocopherol acetate for 42 days, respectively. The results indicated that treatments did not alter growth performance of broilers (p>0.05). Compared with the control group, concentration of ${\alpha}$-tocopherol in the breast muscle was increased by the supplementation of vitamin E (p<0.05). In the thigh, ${\alpha}$-tocopherol content was also enhanced by vitamin E inclusion, and this effect was more pronounced in the natural vitamin E group (p<0.05). Vitamin E supplementation increased the redness of breast (p<0.05). In the contrast, the inclusion of synthetic vitamin E decreased lightness of thigh (p<0.05). Dietary vitamin E inclusion reduced drip loss at 24 h of thigh muscle (p<0.05), and this effect was maintained for drip loss at 48 h in the natural vitamin E group (p<0.05). Broilers given diet supplemented with vitamin E showed decreased malondialdehyde (MDA) content in the breast (p<0.05). Additionally, natural rather than synthetic vitamin E reduced MDA accumulation in the thigh (p<0.05). Neither natural nor synthetic vitamin E supplementation altered muscular mRNA abundance of genes related to oxidative stress (p>0.05). It was concluded that vitamin E supplementation, especially the natural vitamin E, can enhance the retention of muscular ${\alpha}$-tocopherol, improve meat quality and muscular antioxidant capacity of broilers.

• Nutrition Research and Practice
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• v.4 no.5
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• pp.351-355
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• 2010

Our previous proteomic study demonstrated that oxidative stress and antioxidant delphinidin regulated the cellular level of $p27^{kip1}$ (referred to as p27) as well as some heat shock proteins in human colon cancer HT 29 cells. Current study was conducted to validate and confirm the regulation of these proteins using both in vitro and in vivo systems. The level of p27 was decreased by hydrogen peroxide in a dose-dependent manner in human colon carcinoma HCT 116 (p53-positive) cells while it was increased upon exposure to hydrogen peroxide in HT 29 (p53-negative) cells. However, high concentration of hydrogen peroxide (100 ${\mu}M)$ downregulated p27 in both cell lines, but delphindin, one of antioxidative anthocyanins, enhanced the level of p27 suppressed by 100 ${\mu}M$ hydrogen peroxide. ICR mice were injected with varying concentrations of hydrogen peroxide, delphinidin and both. Western blot analysis for the mouse large intestinal tissue showed that the expression of p27 was upregulated by 25 mg/kg BW hydrogen peroxide. To investigate the association of p27 regulation with hypoxia-inducible factor 1-beta (HIF-$1{\beta}$), the level of p27 was analyzed in wild-type mouse hepatoma hepa1c1c7 and Aryl Hydrocarbon Nuclear Translocator (arnt, HIF-$1{\beta}$)-defective mutant BPRc1 cells in the absence and presence of hydrogen peroxide and delphinidin. While the level of p27 was responsive to hydrogen peroxide and delphinidin, it remained unchanged in BPRc1, suggesting that the regulation of p27 requires functional HIF-$1{\beta}$. We also found that hydrogen peroxide and delphinidin affected PI3K/Akt/mTOR signaling pathway which is one of upstream regulators of HIFs. In conclusion, hydrogen peroxide and antioxidant delphinidin seem to regulate intracellular level of p27 through regulating HIF-1 level which is, in turn, governed by its upstream regulators comprising of PI3K/Akt/mTOR signaling pathway. The results should also encourage further study for the potential of p27 as a biomarker for intracellular oxidative or antioxidant status.

• Clinical and Experimental Reproductive Medicine
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• v.41 no.3
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• pp.125-131
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• 2014

Objective: Under estrogen deficiency, blastocysts cannot initiate implantation and enter dormancy. Dormant blastocysts live longer in utero than normal blastocysts, and autophagy has been suggested as a mechanism underlying the sustained survival of dormant blastocysts during delayed implantation. Autophagy is a cellular degradation pathway and a central component of the integrated stress response. Reactive oxygen species (ROS) are produced within cells during normal metabolism, but their levels increase dramatically under stressful conditions. We investigated whether heightened autophagy in dormant blastocysts is associated with the increased oxidative stress under the unfavorable condition of delayed implantation. Methods: To visualize ROS production, day 8 (short-term dormancy) and day 20 (long-term dormancy) dormant blastocysts were loaded with $1-{\mu}M$ 5-(and-6)-chloromethyl-2', 7'-dichlorodihydrofluorescein diacetate, acetyl ester (CM-$H_2DCFDA$). To block autophagic activation, 3-methyladenine (3-MA) and wortmannin were used in vivo and in vitro, respectively. Results: We observed that ROS production was not significantly affected by the status of dormancy; in other words, both dormant and activated blastocysts showed high levels of ROS. However, ROS production was higher in the dormant blastocysts of the long-term dormancy group than in those of the short-term group. The addition of wortmannin to dormant blastocysts in vitro and 3-MA injection in vivo significantly increased ROS production in the short-term dormant blastocysts. In the long-term dormant blastocysts, ROS levels were not significantly affected by the treatment of the autophagy inhibitor. Conclusion: During delayed implantation, heightened autophagy in dormant blastocysts may be operative as a potential mechanism to reduce oxidative stress. Further, ROS may be one of the potential causes of compromised developmental competence of long-term dormant blastocysts after implantation.