Increased oxidative damage with altered antioxidative status in type 2 diabetic patients harboring the 16189 T to C variant of mitochondrial DNA
Increased oxidative damage with altered antioxidative status in type 2 diabetic patients harboring the 16189 T to C variant of mitochondrial DNA
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DOI：
10.1196/annals.1338.007
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发表时间：
2005-01-01
期刊：
影响因子：
--
通讯作者：
Liou, CW
中科院分区：
文献类型：
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作者：
Lin, TK;Chen, SD;Liou, CW
线粒体DNA(MtDNA)16189位核苷酸T到C的转换可能与成人糖尿病的发生有关，因而引起了生物医学研究者的广泛关注。在糖尿病患者中，持续的高血糖可能会导致自由基的大量产生。活性氧被认为在多种生理和病理生理过程中发挥作用，其中氧化应激增加可能在疾病机制中发挥重要作用。本研究的目的是阐明糖尿病患者的氧化损伤程度和血浆抗氧化状态，并观察线粒体DNA 16189变异对这些患者氧化状态的潜在影响。对165例有或无此变异的2型糖尿病患者和168例正常人的血浆脂质过氧化指标丙二醛(MDA)和总游离硫醇进行了测定。在这里，我们报告了与对照组相比，2型糖尿病患者血浆丙二醛和总硫醇水平的增加。线粒体DNA 16189变异型糖尿病患者血浆硫醇水平与对照组无明显差异。这些结果表明，2型糖尿病患者的氧化损伤增加，并处于代偿性更高的抗氧化状态。携带16189线粒体DNA变异体可能会削弱细胞对氧化应激和氧化损伤做出正确反应的能力。
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.