Vascular Risk Factors Plasma Total Antioxidant Activity in Comparison With Plasma NO and VEGF Levels in Patients With Metabolic Syndrome Marcin Barylski, MD, PhD, Edward Kowalczyk, MD, PhD, Maciej Banach, MD, FESC, FASA, FSGC, Julita Ciec ´wierz, MD, PhD, Lucjan Pawlicki, MD, PhD, and Jan Kowalski, MD, PhD Introduction: The aim of our study was to estimate plasma antioxidant activity as well as plasma nitric oxide (NO) and vascular endothelial growth factor levels in patients with metabolic syndrome compared with healthy participants. Material and Methods: Fifty patients (24 women and 26 men, mean age 55.9 + 11.8 years) with metabolic syndrome were compared with 25 healthy participants (12 women and 13 men, mean age 54.2 + 12.8 years). Plasma total antioxidant activity and plasma levels of NO and VEGF were determined in all participants. Results: In the patients with metabolic syndrome, plasma total antioxidant activity, nitric oxide, and vascular endothelial growth factor were significantly lower (P < .001) than that observed in healthy participants (3.2 + 1.6 vs 6.4 + 2.1 mM/L), (6.3 + 2.2 vs 9.8 + 2.7 mM/L), and 71.0 + 16.9 vs 137.5 + 12.6 pg/mL), respectively. Conclusions: Decreased plasma total antioxidant activ- ity, NO, and VEGF levels in patients with metabolic syndrome reflect significant endothelial dysfunction. This suggests that oxidation–reduction balance disorders might play an important role in this process Keywords: metabolic syndrome; plasma total antioxi- dant activity; nitric oxide; vascular endothelial growth factor Introduction Metabolic syndrome (MS) describes the coexistence of the following risk factors for atherosclerosis: atherogenic dyslipidemia, insulin resistance and hyperinsulinemia, hypertension, and obesity. 1,2 Underlying the development of atherosclerotic plaques is a dysfunction of the endothelium that occurs in the course of oxidation–reduction balance disorders. 1-4 In these conditions, vasodilator activity of the endothelium is impaired, which in turn affects the production of nitric oxide (NO). This endothelial dysfunction could affect NO bioavailability due to reduced production and/or increased inactivation of NO. 5 Tissue hypoxia triggers expression of the vascular endothelial growth factor (VEGF) gene, which leads to production of its 3 isoforms (VEGF189, VEGF165, and VEGF121). The VEGF165 isoform is released from cells and circulates in the blood. 6 Blocking NO synthesis inhibits the proliferation of endothelial cells activated by VEGF, 7 and there is a strict relationship between NO and VEGF. 6-8 Nitric oxide induces expression of VEGF, and VEGF has an impact on proliferation of endothelial cells by increasing the synthesis of NO and releasing it directly from endothelial cells. 8 From the Departments of Internal Diseases and Cardiological Rehabilitation (MB, LP, JK), Pharmacology (EK, JC), and Molecular Cardionephrology and Hypertension (MB), Medical University of Lodz, Lodz, Poland. Address correspondence to: Maciej Banach, Department of Molecular Cardionephrology and Hypertension, Medical University of Lodz, Zeromskiego 113, 90-549 Lodz, Poland; e-mail: maciejbanach@aol.co.uk. 87 Angiology Volume 60 Number 1 February/March 2009 87-92 # 2009 SAGE Publications 10.1177/0003319708327165 http://ang.sagepub.com hosted at http://online.sagepub.com by Maciej Banach on April 25, 2015 ang.sagepub.com Downloaded from