P-3：Increased Oxidative Damage with Altered Antioxidative Status in Type 2 Diabetic Patients Harboring the 16189 T to C Variant of Mitochondrial DNA

Tsu-Kung Lin¹, Pei-Wen Wang², Chia-Wei Liou¹, I-Ya Chen², Tzu-Ling Chen³, Cheng-Feng Lee³, Yao-Chung Chuang¹, Shang-Der Chen¹, Yau-Huei Wei³

¹Department of Neurology, ²Metabolism, Chang Gung Memorial Hospital, Kaohsiung, and ³Department of Biochemistry and Center for Cellular and Molecular Biology, National Yang-Ming University, Taipei, Taiwan

ABSTRACT

A transition of T to C at nucleotide position 16189 of mitochondrial DNA (mtDNA) has attracted biomedical researchers for its probable correlation with development of diabetes mellitus (DM) in adult life. In diabetes, persistent hyperglycemia may cause high production of free radicals. Reactive oxygen species (ROS) are thought to play a role in a variety of physiological and pathophysiological processes in which increased oxidative stress may play an important role in disease mechanisms. The aims of the present study were to clarify the degree of oxidative damage and plasma antioxidant status in diabetic patients, and to examine 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 in plasma were measured for 165 type 2 diabetic patients with or without this variant and 168 normal subjects.   Here we report an increase in plasma levels of MDA and total thiols in type 2 diabetic patients compared with normal subjects. The levels of plasma thiols in diabetic patients with the 16189 variant of mtDNA were not different from those of controls.   These results suggest an increase in oxidative damage and a compensatory higher antioxidative status in blood circulation of patients with type 2 diabetes.  Harboring the 16189 variant of mtDNA may impair the ability of the cell to respond properly to oxidative stress and results in oxidative damage.

Keywords: mitochondrial DNA; T16189C polymorphism; type 2 diabetes;

oxidative stress