• Journal of Nutrition and Health
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• v.33 no.2
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• pp.158-166
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• 2000

The effects of smoking and physical exercise on the plasma concentrations of lipid-soluble antioxidants were investigated in 62 healthy males, aged 34-65 years. Current smokers (n=21) and ex-smokers(n=16) had significantly lower plasma levels of carotenoids ($\alpha$-carotene, $\beta$-carotene, cryptoxanthin and lycopene), $\alpha$-tocopherol and ${\gamma}$-tocopherol than non-smokers (n=25). Plasma concentrations of retionl and ubiquinone (coenzyme Q10) were lower among ex-smokers and current smokers than among non-smokers, but the differences were not statistically significant. Regular physical exercise was associated with increased plasma levels of lipid-soluble antioxidants. Plasma concentrations of crytoxanthin, retinol and ubiquinone were significantly elevated in the group engaging in moderate amounts of exercise (more than 20 minutes per day) compared to the group engaging in small amounts of exercise (less than 10 minutes per day). Plasma $\alpha$-carotene, $\beta$-carotene, lycopene levels in the subjects were affected more by smoking than by exercise. However, plasma levels of cryptoxanthin, retinol and ubiquinone in the subjects were affected more by exercise than by smoking. These findings suggest than smoking may cause a decrease in plasma lipid-soluble antioxidants during neutralization of reactive oxygen species present in cigarette smoke and that poor exercise habits may accelerate this imbalance of oxidant/antioxidant homeostasis in middle-aged Korean men.

• Journal of the Korean Society of Food Science and Nutrition
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• v.33 no.1
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• pp.72-77
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• 2004

Diabetic vascular complications such as atherosclerosis have been reported as one of significant obstructions in treatment of diabetes. There has been a significant increase in recognition of the importance of antioxidative nutrients such as vitamin E, for the prevention of diabetic vascular complication by oxidative stress. This study focused on the effect of dietary $\beta$-carotene on the levels of lipid peroxide and antioxidative vitamins of diabetic rats. The plasma glucose level, hepatic level of lipid peroxide and contents of antioxidants such as vitamins A and E were determined in STZ-induced diabetic rats. Dietary supplementation of B-carotene did not reduce the blood glucose in diabetic rats. Hepatic level of lipid peroxide tended to increase in diabetic rats, but $\beta$-carotene intake reduced the value. Plasma levels of retinol and retinol/lipid were not changed by dietary supplementation of $\beta$-carotene. There was no significant difference among experimental groups in plasma level of $\alpha$-tocopherol. Hepatic levels of retionl and retinyl palmitate were increased by dietary supplementation of $\beta$-carotene in diabetic rats. These results suggest that the supplementation of $\beta$-carotene to the normal diet of diabetics may reduce the incidence of the diabetic vascular complications through the improvement of antioxidants depletion.

• Nutritional Sciences
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• v.9 no.1
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• pp.48-54
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• 2006

Methods have been developed to evaluate the total antioxidant capacity of foods and plasma but limitations are associated with their ability to determine precisely the contribution of lipophilic antioxidants in a lipid milieu as well as interactions among them Thus, we modified the Oxygen Radical Absorbance Capacity (ORAC) assay to determine the peroxyradical scavenging ability of both hydrophilic and lipophilic compartments in plasma The hydrophilic ORAC assay was performed in a phosphate buffer system utilizing 2,2'-azobis (2-amidinopropane) dihydrochloride as a peroxyradical generator and fluorescein as the target The lipophilic ORAC assay was carried out in a dimethylsulfoxide :butyronitrile (DMSO/BN, 9:1 v/v) system using 2,2'-azobis (2,4-dimethyl valeronitrile) as a peroxyradical generator and BODIPY C11 581/591 as the target Analyses were conducted in bovine serum supplemented with water - and lipid - soluble antioxidants and in human plasma. Albumin (0.5$\sim$5 g/dL) and uric acid (0.1$\sim$0.5 $\mu$mol/L) increased hydrophilic ORAC values in a dose-dependent fashion ($R^{2}$=0.97 and 0.98, respectively) but had no impact on lipophilic ORAC values. $\alpha$-Tocopherol (15$\sim$200 $\mu$mol/L) increased lipophilic ORAC values in a dose-dependent fashion ($R^{2}$=0.94); neither $\alpha$-tocopherol nor $\beta$-carotene had an impact on hydrophilic ORAC values. However, addition of $\beta$-carotene at physiological concentration (0.23$\sim$1.86 $\mu$mol/L), either alone or in combination with other carotenoids, had no significant impact on lipophilic ORAC values. Thus, while assays of 'total antioxidant capacity' in biological matrices would be a useful research and clinical tool, existing methods are limited by the lack of complete responsiveness to the full range of dietary antioxidants.

• Journal of Nutrition and Health
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• v.44 no.5
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• pp.366-377
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• 2011

Glutathione S-transferase (GST) is a multigene family of phase II detoxifying enzymes that metabolize a wide range of exogenous and endogenous electrophilic compounds. GSTM1 and GSTT1 gene polymorphisms may account for inter-individual variability in coping with oxidative stress. We investigated the relationships between the level of lymphocyte DNA and antioxidative parameters and the effect on GST genotypes. GSTM1 and GSTT1 were characterized in 301 young healthy Korean adults and compared with oxidative stress parameters such as the level of lymphocyte DNA, plasma antioxidant vitamins, and erythrocyte antioxidant enzymes in smokers and non smokers. GST genotype, degree of DNA damage in lymphocytes, erythrocyte activities of superoxide dismutase, catalase, and glutathione peroxidase (GSH-Px), and plasma concentrations of total radical-trapping antioxidant potential (TRAP), vitamin C, ${\alpha}$- and ${\gamma}$-tocopherol, ${\alpha}$- and ${\beta}$-carotene, and cryptoxanthin were analyzed. Lymphocyte DNA damage assessed by the comet assay was higher in smokers than that in non-smokers, but the levels of plasma vitamin C, ${\beta}$-carotene, TRAP, erythrocyte catalase, and GSH-Px were lower than those of non-smokers (p < 0.05). Lymphocyte DNA damage was higher in subjects with the GSTM1- or GSTT1-present genotype than those with the GSTM1-present or GSTT1- genotype. No difference in erythrocyte antioxidant enzyme activities, plasma TRAP, or vitamin levels was observed in subjects with the GSTM1 or GSTT1 genotypes, except ${\beta}$-carotene. Significant negative correlations were observed between lymphocyte DNA damage and plasma levels of TRAP and erythrocyte activities of catalase and GSH-Px after adjusting for smoking pack-years. Negative correlations were observed between plasma vitamin C and lymphocyte DNA damage only in individuals with the GSTM1-present or GSTT1- genotype. The interesting finding was the significant positive correlations between lymphocyte DNA damage and plasma levels of ${\alpha}$-carotene, ${\beta}$-carotene, and cryptoxanthin. In conclusion, the GSTM1- and GSTT1-present genotypes as well as smoking aggravated antioxidant status through lymphocyte DNA damage. This finding confirms that GST polymorphisms could be important determinants of antioxidant status in young smoking and non-smoking adults. Consequently, the protective effect of supplemental antioxidants on DNA damage in individuals carrying the GSTM1- or GSTT1-present genotypes might show significantly higher values than expected.

• Journal of Nutrition and Health
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• v.29 no.2
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• pp.223-231
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• 1996

To investigate antioxidant status and platelet antioxidative enzyme activity in patients with ischemic heart disease, 36 male patients admitted to Kyungpook National University Hospital from June to December 1994 were compared to 36 healthy male control subjects. The percentages of heavy smoking and nonexercise were significantly higher in the patient group compared to the control, but the drinking status was not significantly different between groups. Food habit and food frequency scores were significantly lower in patients than in control subjects. Plasma retinol levels tended to be lower in the patient group, and plasma $\alpha$-tocopherol and $\beta$-carotene levels were not different between groups. There was no difference in the level of plasma thiobarbituric acid reactive substances(TBARS) and in the activities of platelet glutathione peroxidase and catalase. Our results indicate that oxidative stress, which is reflected by the plasma levels of antioxidants and TBARS, did not increase in the patients with ischemic heart disease, and the long-term effects due to smoking, poor food habit and other life styles could possibly contribute to the onset of the disease.

• Journal of the Korean Society of Food Science and Nutrition
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• v.36 no.6
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• pp.708-719
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• 2007

Glutathione S-transferase genotypes GSTT1, GSTM1 and GSTP1 were characterized in 104 healthy male and female subjects and compared with parameters of oxidative stress at the level of DNA and lipids, with antioxidant enzymes, and with plasma antioxidants in smokers and non.smokers. Of the 104 subjects studied, 57.4% were GSTT1 present and 47.6% were GSTM1 present. The GSTP1 polymorphisms a and b were represented as follows: a/a, 75.5%; a/b, 21.6%; b/b type, 2.9%. The GSTT1 null genotype was associated with decreased glutathione in erythrocytes and elevated lymphocytes DNA damage. GST-Px was higher in GSTT1 null compared with GSTT1 present type. The homozygous GSTP1 genotype was not associated with any antioxidant status or DNA damage. The difference in plasma ${\alpha}$-carotene and erythrocytes GSH-Px and GST activities between smokers and non-smokers was detected in the GSTT1 null genotype. Plasma ${\gamma}$-tocopherol and ${\beta}$-carotene decreased significantly in smokers having GSTM1 null genotype. When GSTT1 and GSTM1 were combined, plasma lycopene and erythrocyte GST were reduced in smokers in both null types of these genes. As for GSTP1 genotype, plasma ${\alpha}$-carotene and erythrocytes GSH-Px decreased significantly in smokers with GSTP1 b/b, while erythrocytes GSH-Px activities decreased in smokers with GSTP1 a/b. The different ${\beta}$-carotene level between smokers and non-smokers was seen with both GSTP1 a/a and a/b genotype. It seems that polymorphisms in the phase II metabolizing enzyme glutathione S-transferase may be important determinants of commonly measured biomarkers.

• Journal of the Korean Society of Food Science and Nutrition
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• v.24 no.6
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• pp.848-858
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• 1995

The present study was conducted to investigate the effect of dietary vitamin A on the antioxidant status in ethanol-treated rats. Weaning rats were fed a basal diet until they reached about 160-180g body weight. Thereafter, four experimental groups were fed a liquid diet containing 36% ethanol of total calorie and four pair-fed groups were fed isocaloric sucorse instead of ethanol. Additionally, the liquid diet contained adequate amount of ${\beta}-carotene$, retinyl acetate, or 13-cis-retinoic acid except vitamin A deficient diet. The rats were sacrificed after 7 weeks of feedng periods. Significant decrease in hepatic vitamin E content was found in rats treated with chronic ethanol. However, dietary supplementation of retinyl acetate modified the change to some extent. Total vitamin C content of liver increased in vitamin A-deficient or ${\beta}-carotene$ groups with ethanol feeding. The ratio of reduced/oxidized vitamin C increased in the plasma and liver of ${\beta}-carotene$ group with ethanol feeding. Chronic ethanol intake did not change the total glutathione content of rat liver, but increased reduced glutathione(GSH)/oxidized glutathione(GSSG) ratio. This increase in hepatic GSH after chronic ethanol treatment. The changes of Se content in plasma and liver was not consistant. Fe content of liver increased by ethanol treatment, but this increase reduced in rats fed dietary retinyl acetate or 13-cis-retinoic acid. Fe content of plasma increased in vitamin A-deficient and ${\beta}-carotene$ supplemented groups with ethanol intake.

• 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.