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Increased Oxidative Damage with Altered Antioxidative Status in Type 2 Diabetic Patients Harboring the 16189 T to C Variant of Mitochondrial DNA
Author(s) -
LIN TSUKUNG,
CHEN SHANGDER,
WANG PEIWEN,
WEI YAUHUEI,
LEE CHENGFENG,
CHEN TZULING,
CHUANG YAOCHUNG,
TAN TENGYEOW,
CHANG KUCHOU,
LIOU CHIAWEI
Publication year - 2005
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1338.007
Subject(s) - oxidative stress , lipid peroxidation , malondialdehyde , diabetes mellitus , oxidative phosphorylation , mitochondrial dna , reactive oxygen species , medicine , endocrinology , dna damage , type 2 diabetes , mitochondrion , oxidative damage , chemistry , antioxidant , biochemistry , dna , gene
A bstract : A transition of T to C at nucleotide position 16189 in mitochondrial DNA (mtDNA) has attracted biomedical researchers for its probable correlation with the development of diabetes mellitus in adult life. In diabetes, persistent hyperglycemia may cause high production of free radicals. Reactive oxygen species are thought to play a role in a variety of physiologic and pathophysiologic processes in which increased oxidative stress may play an important role in disease mechanisms. The aim of the present study was to clarify the degree of oxidative damage and plasma antioxidant status in diabetic patients and to see the potential influence of the 16189 variant of mtDNA on the oxidative status in these patients. An indicative parameter of lipid peroxidation, malondialdehyde (MDA), and total free thiols were measured from plasma samples of 165 type 2 diabetic patients with or without this variant and 168 normal subjects. Here we report an increase in the plasma levels of MDA and total thiols in type 2 diabetic patients compared with control subjects. The levels of plasma thiols in diabetic patients with the 16189 variant of mtDNA were not different from those in controls. These results suggest an increase in the oxidative damage and a compensatory higher antioxidative status in patients with type 2 diabetes. Harboring the 16189 mtDNA variant may impair the ability of a cell to respond properly to oxidative stress and oxidative damage.