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      Effects of glutathione s-transferase ( GST) M1 and T1 polymorphisms on antioxidant vitamins and oxidative stress-related parameters in Korean subclinical hypertensive subjects after kale juice ( Brassica oleracea acephala) supplementation

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          Abstract

          BACKGROUND/OBJECTIVES

          Glutathione s-transferase ( GST) is involved in the formation of a multigene family comprising phase II detoxification enzymes, involved in the detoxification of reactive oxygen species. This study evaluated whether daily supplementation with kale juice could modulate levels of plasma antioxidant vitamins and oxidative stress-related parameters. We further examined whether this modulation was affected by combined GSTM1 and T1 polymorphisms.

          SUBJECTS/METHODS

          Totally, 84 subclinical hypertensive patients having systolic blood pressure (BP) over 130 mmHg or diastolic BP over 85 mmHg, received 300 mL of kale juice daily for 6 weeks. Blood samples were drawn before start of study and after completion of 6 weeks.

          RESULTS

          After supplementation, we observed significant decrease in DNA damage and increase in erythrocyte catalase activity in all genotypes. Plasma level of vitamin C was significantly increased in the wild/null and double null genotypes. The plasma levels of β-carotene, erythrocyte glutathione peroxidase activity, and nitric oxide were increased only in the wild/null genotype after kale juice supplementation.

          CONCLUSIONS

          The effect of kale juice was significantly greater in the GSTM1 null genotype and wild/null genotype groups, suggesting possibility of personalized nutritional prescriptions based on personal genetics.

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          Most cited references40

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          Glutathione transferases.

          This review describes the three mammalian glutathione transferase (GST) families, namely cytosolic, mitochondrial, and microsomal GST, the latter now designated MAPEG. Besides detoxifying electrophilic xenobiotics, such as chemical carcinogens, environmental pollutants, and antitumor agents, these transferases inactivate endogenous alpha,beta-unsaturated aldehydes, quinones, epoxides, and hydroperoxides formed as secondary metabolites during oxidative stress. These enzymes are also intimately involved in the biosynthesis of leukotrienes, prostaglandins, testosterone, and progesterone, as well as the degradation of tyrosine. Among their substrates, GSTs conjugate the signaling molecules 15-deoxy-delta(12,14)-prostaglandin J2 (15d-PGJ2) and 4-hydroxynonenal with glutathione, and consequently they antagonize expression of genes trans-activated by the peroxisome proliferator-activated receptor gamma (PPARgamma) and nuclear factor-erythroid 2 p45-related factor 2 (Nrf2). Through metabolism of 15d-PGJ2, GST may enhance gene expression driven by nuclear factor-kappaB (NF-kappaB). Cytosolic human GST exhibit genetic polymorphisms and this variation can increase susceptibility to carcinogenesis and inflammatory disease. Polymorphisms in human MAPEG are associated with alterations in lung function and increased risk of myocardial infarction and stroke. Targeted disruption of murine genes has demonstrated that cytosolic GST isoenzymes are broadly cytoprotective, whereas MAPEG proteins have proinflammatory activities. Furthermore, knockout of mouse GSTA4 and GSTZ1 leads to overexpression of transferases in the Alpha, Mu, and Pi classes, an observation suggesting they are part of an adaptive mechanism that responds to endogenous chemical cues such as 4-hydroxynonenal and tyrosine degradation products. Consistent with this hypothesis, the promoters of cytosolic GST and MAPEG genes contain antioxidant response elements through which they are transcriptionally activated during exposure to Michael reaction acceptors and oxidative stress.
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            A simple technique for quantitation of low levels of DNA damage in individual cells.

            Human lymphocytes were either exposed to X-irradiation (25 to 200 rads) or treated with H2O2 (9.1 to 291 microM) at 4 degrees C and the extent of DNA migration was measured using a single-cell microgel electrophoresis technique under alkaline conditions. Both agents induced a significant increase in DNA migration, beginning at the lowest dose evaluated. Migration patterns were relatively homogeneous among cells exposed to X-rays but heterogeneous among cells treated with H2O2. An analysis of repair kinetics following exposure to 200 rads X-rays was conducted with lymphocytes obtained from three individuals. The bulk of the DNA repair occurred within the first 15 min, while all of the repair was essentially complete by 120 min after exposure. However, some cells demonstrated no repair during this incubation period while other cells demonstrated DNA migration patterns indicative of more damage than that induced by the initial irradiation with X-rays. This technique appears to be sensitive and useful for detecting damage and repair in single cells.
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              Pathogenesis of hypertension.

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                Author and article information

                Journal
                Nutr Res Pract
                Nutr Res Pract
                NRP
                Nutrition Research and Practice
                The Korean Nutrition Society and the Korean Society of Community Nutrition
                1976-1457
                2005-6168
                April 2018
                22 March 2018
                : 12
                : 2
                : 118-128
                Affiliations
                [1 ]Department of Food and Nutrition, College of Life Science and Nano Technology, Hannam University, 461-6 Jeonmin-dong, Yuseong-gu, Daejeon 34054, Korea.
                [2 ]Nutrition Safety Policy Division, Ministry of Food and Drug Safety, Chungbuk 28159, Korea.
                [3 ]Department of Medical Nutrition, Graduate School of East-West Medical Science, Kyung Hee University, 1732 Deogyeong-daero, Giheung-gu, Yongin-si, Gyeonggi 17104, Korea.
                Author notes
                Corresponding Authors: Myung-Hee Kang, Tel. 82-53-629-8791, Fax. 82-42-629-8808, mhkang@ 123456hnu.kr
                Corresponding Authors: Yoo Kyoung Park, Tel. 82-31-201-3816, Fax. 82-31-203-3816, ypark@ 123456khu.ac.kr

                *These authors contributed equally to this work.

                Author information
                https://orcid.org/0000-0003-4127-9952
                https://orcid.org/0000-0002-9058-6193
                https://orcid.org/0000-0002-8536-0835
                https://orcid.org/0000-0003-2647-1831
                Article
                10.4162/nrp.2018.12.2.118
                5886963
                29629028
                88fa2658-b8d6-466e-b17e-9753e2937def
                ©2018 The Korean Nutrition Society and the Korean Society of Community Nutrition

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 03 August 2017
                : 25 September 2017
                : 19 February 2018
                Funding
                Funded by: National Research Foundation of Korea, CrossRef http://dx.doi.org/10.13039/501100003725;
                Award ID: 2010-0012031
                Categories
                Original Research

                Nutrition & Dietetics
                kale,hypertension,dna damage,genotype,oxidative stress
                Nutrition & Dietetics
                kale, hypertension, dna damage, genotype, oxidative stress

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