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Oxidative risk for atherothrombotic cardiovascular disease.

ABSTRACT: In the vasculature, reactive oxidant species, including reactive oxygen, nitrogen, or halogenating species, and thiyl, tyrosyl, or protein radicals may oxidatively modify lipids and proteins with deleterious consequences for vascular function. These biologically active free radical and nonradical species may be produced by increased activation of oxidant-generating sources and/or decreased cellular antioxidant capacity. Once formed, these species may engage in reactions to yield more potent oxidants that promote transition of the homeostatic vascular phenotype to a pathobiological state that is permissive for atherothrombogenesis. This dysfunctional vasculature is characterized by lipid peroxidation and aberrant lipid deposition, inflammation, immune cell activation, platelet activation, thrombus formation, and disturbed hemodynamic flow. Each of these pathobiological states is associated with an increase in the vascular burden of free radical species-derived oxidation products and, thereby, implicates increased oxidant stress in the pathogenesis of atherothrombotic vascular disease.

SUBMITTER: Leopold JA

PROVIDER: S-EPMC2797369 | biostudies-other | 2009 Dec

REPOSITORIES: biostudies-other

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Oxidative risk for atherothrombotic cardiovascular disease.

Leopold Jane A JA Loscalzo Joseph J

Free radical biology & medicine 20090912 12

In the vasculature, reactive oxidant species, including reactive oxygen, nitrogen, or halogenating species, and thiyl, tyrosyl, or protein radicals may oxidatively modify lipids and proteins with deleterious consequences for vascular function. These biologically active free radical and nonradical species may be produced by increased activation of oxidant-generating sources and/or decreased cellular antioxidant capacity. Once formed, these species may engage in reactions to yield more potent oxid ...[more]

PMID: 19751821

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Project description: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.

Dataset Information

Oxidative risk for atherothrombotic cardiovascular disease.

Publications

Oxidative risk for atherothrombotic cardiovascular disease.

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