###### Abstract  
Metabolic syndrome (MetS) is defined by the World Health Organisation (WHO) as a pathologic condition characterized by abdominal obesity, insulin resistance, hypertension, and hyperlipidemia. The components of MetS and the associated cardiovascular risks may disrupt the vascular endothelial function and the structure of the vascular wall, increasing the risk of atherosclerosis and vascular diseases. In this study we evaluated the relationship between the carotid intima-media thickness (CIMT), the redox balance parameters of plasma asymmetric dimethylarginine (ADMA), malondialdehydedebyde (MDA), and heme oxygenase 1 (HO-1), and the expression of oxidative stress-related nuclear factor kappa B (NF-kB), nuclear factor erythroid 2-related factor 2 (Nrf2), and HO-1 in peripheral blood mononuclear cells (PBMCs) in MetS. Significantly higher CIMT was established in MetS patients aged \(\geq\) 55 years as compared with the control group (0.96 \(\pm\) 0.29 vs. 0.74 \(\pm\) 0.21, \(p\) < 0.05). Expression was higher in MetS patients aged \(<\) 55 years (83% for NF-kB, \(p\) < 0.05, 251% for Nrf2, \(p\) < 0.05, and 337% for HO-1, \(p\) < 0.05) in comparison to the control group. Similarly, expression was higher in CIMT \(<\) 0.90 mm than the control group by 80% for NF-kB, \(p\) < 0.01; 260% for Nrf2, \(p\) < 0.05, and 303% for HO-1, \(p\) < 0.05. In contrast, gene expression was under-regulated in the subgroups of MetS patients aged \(\geq\) 55 years and MetS patients with CIMT \(\geq\) 0.90 mm. Significantly higher plasma levels for MDA, \(\Delta\)DMA, and HO-1 were established in the age \(<\) 55 and age \(\geq\) 55 MetS subgroups and the CIMT \(<\) 0.90 mm and CIMT \(\geq\) 0.90 mm subgroups. In conclusion, MetS individuals aged \(\geq\) 55 are at higher risk of increased CIMT and impaired redox balance. e-Associated Changes in Carotid Intima-Media Thickness in Relation to Redox Balance Indices in Metabolic Syndrome  
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Aticle Age-Associated Changes in Carotid Intima-Media Thickness in Relation to Redox Balance Indices in Metabolic Syndrome  
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and hyperlipidaemia [1]. The components of MetS and the associated cardiovascular risks may disrupt the vascular endothelial function and the structure of the vascular wall, increasing the risk of atherosclerosis and vascular diseases [2]. Endothelial dysfunction (ED) is one of the major factors in the pathogenesis of MetS and atherosclerosis [3;4]. Recently, asymmetric dimethylarginine (ADMA), which is an endogenous inhibitor of nitric oxide synthetase and NO, was described as an emerging cardiovascular risk factor [5;6]. Carotid intima-media thickness (CIMT) and ADMA are currently widely used markers for ED and increased risk of cardiovascular diseases (CVDs) and atherosclerosis [7; 8; 9]. The ED molecular mechanisms in MetS are not completely understood, but free radicals and inflammatory mediators are thought to be involved. Oxidative stress and inflammation induced by high low-density lipoproteins (LDL) or by tumour necrosis factor alpha (TNF-alpha) increase plasma ADMA [3]. Previous studies have demonstrated that ADMA could lead to a concentration-dependent increase in the production of reactive oxygen species (ROS), which act as second messengers and activate nuclear factor kappa B (NF-kB) in endothelial cells [10]. Oxidative stress is a predominant factor for endothelial cell activation and dysfunction and oxidative stress-induced endothelial cell injury. The transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) is well recognized as a critical regulator of redox and metabolic homeostasis and an inflammation regulator as well [11;12]. Nrf2, a redox-sensitive transcription factor, increases the expression of heme oxygenase 1 (HO-1) and other genes [11], playing an important role in endothelial protection against oxidative stress [12]. HO-1 is expressed at low levels in endothelial cells and white blood cells under physiological conditions. It is highly inducible in response to stress [13].