Hernandez-Mijares 2011 Free Radic Biol Med

Hernandez-Mijares A, Rocha M, Apostolova N, Borras C, Jover A, Bañuls C, Sola E, Victor VM (2011) Mitochondrial complex I impairment in leukocytes from type 2 diabetic patients. Free Radic Biol Med 50:1215-21.

» PMID: 21262346

Hernandez-Mijares A, Rocha M, Apostolova N, Borras C, Jover A, Banuls C, Sola E, Victor VM (2011) Free Radic Biol Med

Abstract: 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 mitochondrial oxygen (O₂) 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-α), 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 mitochondrial function in diabetic patients, evidenced by a decrease in mitochondrial O₂ 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 mitochondrial complex I.

Labels: MiParea: Patients Pathology: Diabetes Stress:Oxidative stress;RONS

Tissue;cell: Macrophage-derived

Enzyme: Complex I