Mitochondrial complex I impairment in leukocytes from type 2 diabetic patients

作者：Hernandez Mijares Antonio; Rocha Milagros; Apostolova Nadezda; Borras Consuelo; Jover Ana; Banuls Celia; Sola Eva; Victor Victor M^*

来源：Free Radical Biology and Medicine, 2011, 50(10): 1215-1221.

DOI：10.1016/j.freeradbiomed.2011.01.019

• Antioxidant
• Complex I
• Diabetes
• Mitochondria
• Oxidative stress
• Reactive oxygen species
• Free radicals

Diabetes is associated with oxidative stress. This study evaluated the rates of oxidative stress and mitochondrial impairment in type 2 diabetes patients. The study population consisted of 182 diabetic patients and 50 body-composition- and age-matched controls. We assessed anthropometric and metabolic parameters and mitochondrial function by evaluating mitochondria' oxygen (O(2)) consumption, reactive oxygen species (ROS) production, glutathione (GSH) levels, GSH/GSSG ratio, mitochondrial membrane potential, and mitochondrial complex I activity in polymorphonuclear cells from diabetes type 2 patients. We found an increase in waist circumference and augmented serum levels of triglycerides, proinflammatory cytokines (IL-6 and TNF-alpha), homocysteine, glycated hemoglobin, ultrasensitive C-reactive protein, glucose, insulin, and homeostasis model assessment of insulin resistance score in diabetic patients versus controls. There was an impairment of mitochondria' function in diabetic patients, evidenced by a decrease in mitochondrial O(2) consumption, an increase in ROS production, decreased GSH/GSSG ratio, a drop in GSH levels, and an undermining of the mitochondrial membrane potential. Furthermore, an impairment of mitochondrial complex I was detected. This study supports the hypothesis of an association of type 2 diabetes and the rate of impaired mitochondrial function. We also propose that one of the targets of oxidative stress responsible for diabetes is mitochondria' complex I.

• 出版日期2011-5-15