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KMID : 0381020110440010016
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Korean Journal of Nutrition
2011 Volume.44 No. 1 p.16 ~ p.28
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Antioxidative Status, DNA Damage and Lipid Profiles in Korean Young Adults by Glutathione S-Transferase Polymorphisms
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Jo Hye-Ryun
Lee Hye-Jin
Kang Myung-Hee
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Abstract
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Oxidative stress leads to the induction of cellular oxidative damage, which may cause adverse modifications of DNA, proteins, and lipids. The production of reactive species during oxidative stress contributes to the pathogenesis of many diseases. Antioxidant defenses can neutralize reactive oxygen species and protect against oxidative damage. The aim of this study was to assess the antioxidant status and the degree of DNA damage in Korean young adults using glutathione s-transferase (GST) polymorphisms. The GSTM1 and GSTT1 genotypes were characterized in 245 healthy young adults by smoking status, and their oxidative DNA damage in lymphocytes and antioxidant status were assessed by GST genotype. General characteristics were investigated by simple questionnaire. From the blood of the subjects, GST genotypes; degree of DNA damage in lymphocytes; the erythrocyte activities of superoxide dismutase, catalase, and glutathione peroxidase; plasma concentrations of total peroxyl radical-trapping potential (TRAP), vitamin C, α- and γ-tocopherol, α- and β-carotene and cryptoxanthin, as well as plasma lipid profiles, conjugated diene (CD), GOT, and GPT were analyzed. Of the 245 subjects studied, 23.2% were GSTM1 wild genotypes and 33.4% were GSTT1 wild genotype. No difference in erythrocyte activities of superoxide dismutase, catalase, or glutathione peroxidase, and the plasma TRAP level, CD, GOT, and GPT levels were observed between smokers and non-smokers categorized by GSTM1 or GSTT1 genotype. Plasma levels of α- and γ-tocopherol increased significantly in smokers with the GSTT1 wild genotype (p < 0.05); however, plasma level of α-carotene decreased significantly in non-smokers with the GSTM1 wild genotype (p < 0.05). DNA damage assessed by the Comet assay was significantly higher in non-smokers with the GSTM1 null genotype; whereas DNA damage was significantly lower in non-smokers with the GSTT1 null genotype. Total cholesterol and LDL cholesterol levels were significantly higher in non-smokers with the GSTT1 null genotype than those with the GSTT1 wild genotype (p < 0.05). In conclusion, the GSTM1 null genotype or the GSTT1 wild genotype in non-smokers aggravated their antioxidant status through DNA damage of lymphocytes; however, the GSTT1 wild type in non-smokers had normal plasma total cholesterol and LDL-cholesterol levels. This finding confirms that GST polymorphisms could be an important determinant of antioxidant status and plasma lipid profiles in non-smoking young adults. Further study is necessary to clarify the antioxidant status and/or lipid profiles of smokers with the GST polymorphism and to conduct a study with significantly more subjects.
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KEYWORD
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oxidative stress, GST polymorphisms, antioxidative status, DNA damage, lipid profiles
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