Abstract
The objective of the study was to evaluate oxidative stress (OS) status in subjects with different cardiovascular risk factors. With this in mind, we have studied three models of high cardiovascular risk: hypertension (HT) with and without metabolic syndrome, familial hypercholesterolemia (FH) and familial combined hyperlipidemia (FCH) with and without insulin resistance. Oxidative stress markers (oxidized/reduced glutathione ratio, 8-oxo-deoxyguanosine and malondialdehide) together with the activity of antioxidant enzyme triad (superoxide dismutase, catalase, glutathione peroxidase) and activation of both pro-oxidant enzyme (NAPDH oxidase components) and AGTR1 genes, as well as antioxidant enzyme genes (CuZn-SOD, CAT, GPX1, GSR, GSS and TXN) were measured in mononuclear cells of controls (n = 20) and patients (n = 90) by assessing mRNA levels. Activity of some of these antioxidant enzymes was also tested. An increase in OS and pro-oxidant gene mRNA values was observed in patients compared to controls. The hypertensive group showed not only the highest OS values, but also the highest pro-oxidant activation compared to those observed in the other groups. In addition, in HT a significantly reduced antioxidant activity and mRNA induction of antioxidant genes were found when compared to controls and the other groups. In FH and FCH, the activation of pro-oxidant enzymes was also higher and antioxidant ones lower than in the control group, although it did not reach the values obtained in hypertensives. The thioredoxin system was more activated in patients as compared to controls, and the highest levels were in hypertensives. The increased oxidative status in the presence of cardiovascular risk factors is a consequence of both the activation of pro-oxidant mechanisms and the reduction of the antioxidant ones. The altered response of the main cytoplasmic antioxidant systems largely contributes to OS despite the apparent attempt of the thioredoxin system to control it.
Highlights
An excessive production of reactive oxygen species (ROS) outstripping antioxidant defense mechanisms has been implicated in conditions which impact the cardiovascular system and the development of atherosclerosis [1,2]
The study was performed in 90 patients with CV risk factors (43 HT, 17 familial hypercholesterolemia (FH) and 30 familial combined hyperlipidemia (FCH)) and 20 control volunteers
The characteristics of each group of patients and controls are shown in Table 1 and in Table S2 for patients grouped by metabolic syndrome (MS) or insulin resistance (IR)
Summary
An excessive production of reactive oxygen species (ROS) outstripping antioxidant defense mechanisms has been implicated in conditions which impact the cardiovascular system and the development of atherosclerosis [1,2]. The increased oxidative stress (OS) is driven by the presence of the so-called cardiovascular (CV) risk factors and their impact on both pro-oxidant and antioxidant mechanisms. In a previous study carried out in hypertensive patients by our group, we observed that both blood and peripheral mononuclear cells exhibit important deficiencies of physiological antioxidants with a deep reduction in enzymatic activity and GSH levels [9]. Mechanisms underlying these alterations are not well understood, but an increase in activity of pro-oxidant enzymes, mainly NADPH oxidase that can be activated by angiotensin II through Angiotensin AT1 receptor (AGTR1)
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