Nutr Res Pract.  2017 Jun;11(3):214-222. 10.4162/nrp.2017.11.3.214.

Lymphocyte DNA damage and plasma antioxidant status in Korean subclinical hypertensive patients by glutathione S-transferase polymorphism

Affiliations
  • 1Nutrition Safety Policy Division, Food Nutrition and Dietary Safety Bureau, Ministry of Food and Drug Safety, Heungdeok-gu, Cheongju-si, Chungbuk 28159, Korea.
  • 2Department of Food Science and Nutrition, Daedeok Valley Campus, Hannam University, 461-6 Jeonmin-dong, Yuseong-gu, Daejeon 34054, Korea. mhkang@hnu.kr
  • 3Department of Family Medicine, Eulji University School of Medicine, Daejeon 35233, Korea.
  • 4Center for Cohort Studies, Total Healthcare Center, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul 03181, Korea.

Abstract

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) ≥ 130 mmHg or diastolic BP ≥ 85 mmHg) 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 α-tocopherol increased significantly in GSTT1 wild genotype (P < 0.05); however, plasma level of β-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.

Keyword

Glutathione S-transferase; hypertension; DNA damage; oxidative stress; antioxidants

MeSH Terms

Antioxidants
Blood Pressure
Catalase
Comet Assay
DNA Damage*
DNA*
Erythrocytes
Genotype
Glutathione Peroxidase
Glutathione Transferase*
Glutathione*
Humans
Hypertension
Korea
Lymphocytes*
Metabolic Detoxication, Phase II
Multigene Family
Oxidative Stress
Plasma*
Superoxide Dismutase
Vitamins
Xenobiotics
Antioxidants
Catalase
DNA
Glutathione
Glutathione Peroxidase
Glutathione Transferase
Superoxide Dismutase
Vitamins
Xenobiotics

Figure

  • Fig. 1 Level of plasma (A) TRAP, (B) β-carotene, (C) α-tocopherol and (D) lymphocyte DNA damage reflected by tail length according to the GSTM1/GSTT1 combined genotype, and each genotype in the hypertensive patients. Values with different letters within a row are significantly different at P < 0.05 after Scheffe test followed by ANOVA. *P < 0.05, **P < 0.01


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