Effects of combined dietary supplementation on oxidative and inflammatory status in dyslipidemic subjects

Accinni, R.; Rosina, Marco; Bamonti, Fabrizia; Noce, Cinzia Della; Tonini, A.; Bernacchi, F.; Campolo, Jonica; Caruso, Raffaele; Novembrino, Cristina; Ghersi, L.; Lonati, Silvia; Grossi, Sara G.; Ippolito, Silvia; Lorenzano, Elettra; Ciani, Aldo; Gorini, Marco

doi:10.1016/j.numecd.2005.05.006

Cited by 56 publications

(25 citation statements)

References 34 publications

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“…The effects of marine n-3 fatty acids on circulating inflammatory markers among individuals with a high risk of developing CVD are shown in Table 3 [35–49] . Four of fifteen trials reported a reduction in the concentration of inflammatory markers after intake of marine n-3 fatty acids [35, 36, 45, 46], while nine studies did not observe any effects on inflammation [37–44, 48]. An increase in inflammatory markers [49] was reported in one study.…”

Section: Resultsmentioning

confidence: 99%

Effect of marine n-3 fatty acids on circulating inflammatory markers in healthy subjects and subjects with cardiovascular risk factors

et al. 2011

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ObjectiveThe aim of the present paper was to review the literature in order to summarize the effects of marine n-3 fatty acids on circulating inflammatory markers among healthy subjects, subjects with high risk of developing cardiovascular disease (CVD) and in patients with CVD in human intervention studies.MethodsA systematic literature search in PubMed was performed. Intervention studies describing the effects of marine n-3 fatty acids on circulating inflammatory markers in healthy subjects, subjects with high risk of CVD and patients with CVD were included. The following exclusion criteria were used: (1) interventions assessing inflammatory markers with ex vivo methods (2) interventions with children (3) articles describing animal or cell culture studies. Twenty-two articles were included. Additionally, 13 papers from their literature lists were included based on the same inclusion and exclusion criteria as the literature search.Results and conclusionIntervention studies with marine n-3 fatty acids administered from either fish or fish oil demonstrate different results on inflammatory markers. No firm conclusion can be drawn about the effect of marine n-3 fatty acids on circulating inflammatory markers in healthy individuals, individuals with high risk of developing CVD or individuals with CVD related diseases.

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Section: Resultsmentioning

confidence: 99%

Effect of marine n-3 fatty acids on circulating inflammatory markers in healthy subjects and subjects with cardiovascular risk factors

et al. 2011

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“…Another positive clinical study used a combination of antioxidants (NAC, Vitamin E (VitE) and Vitamin C (VitC)) to treat young (mean age 41) diabetic patients or patients with impaired glucose tolerance (IGT), and found a reduction of oxidative stress and inflammation after 15 days of treatment (Neri et al 2005). The combination of VitE, fish oil, niacin and γ-oryzanol showed a beneficial effect in reducing oxidative stress and inflammatory markers in young dyslipidemic patients (Accinni et al 2006). However, overwhelmingly, clinical trials have failed to show a protective effect of antioxidants in humans.…”

Section: Discussionmentioning

confidence: 99%

Basic Mechanisms of Oxidative Stress and Reactive Oxygen Species in Cardiovascular Injury

Papaharalambus

Griendling

2007

Trends in Cardiovascular Medicine

290

224

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The development of vascular disease has its origins in an initial insult to the vessel wall by biological or mechanical factors. The disruption of homeostatic mechanisms leads to alteration of the original architecture of the vessel and its biological responsiveness, contributing to acute or chronic diseases such as stroke, hypertension and atherosclerosis. Endothelial dysfunction, macrophage infiltration of the vessel wall, and proliferation and migration of smooth muscle cells all involve different types of reactive oxygen species, produced by various vessel wall components. Although basic science and animal research have clearly established the role of reactive oxygen species in the progression of vascular disease, the failure of clinical trials with antioxidant compounds has underscored the need for better antioxidant therapies and a more thorough understanding of the role of reactive oxygen species in cardiovascular physiology and pathology.The fundamental processes underlying the development of vascular diseases such as atherosclerosis, restenosis and hypertensive vascular remodeling have their origins in an initial insult to the vessel wall. Such an insult may arise from mechanical disruption that occurs during percutaneous coronary angioplasty or at regions of oscillatory shear stress, or it can result from biological causes, such as hypercholesterolemia, excess free radicals, diabetes, increased concentrations of plasma homocysteine, or infectious agents. Injury promotes disruption of the homeostatic mechanisms of the endothelial protective barrier, changing its natural properties, increasing its adhesiveness to leukocytes and altering its permeability. This endothelial dysfunction also leads to the formation of vasoactive molecules, which in turn induce inflammatory genes, inactivate nitric oxide (NO • ) and its protective functions, and activate matrix metalloproteinases, leading to extracellular matrix remodeling, and increased smooth muscle cell (VSMC) growth, migration and proliferation. Each of these processes contributes to thickening of the vessel wall or the formation of lesions that can lead to hypertension, acute myocardial infarction and stroke. Reactive Oxygen Species and Vascular InjuryIn the past decade a staggering amount of evidence implicates a common denominator, reactive oxygen species (ROS), in the development of most cardiovascular diseases (Figure 1). Superoxide (O 2 •− ) and hydrogen peroxide (H 2 O 2 ) are two of the most biologically important ROS in the cardiovascular system, and are produced in vascular cells by a number of oxidases, including the NADPH oxidases (Nox) and xanthine oxidase, lipoxygenases, cytochrome p450,

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“…Oxidation susceptibility of n-3 PUFA requires to be counterbalanced by antioxidants. In-vivo human studies conducted in dyslipidemic subjects, have effectively demonstrated the positive potentials in combining n-3 PUFA dietary supplementation with vitamin E, niacin and c-oryzanol to improve the lipid pattern, decrease serum ROS concentration and increase the total antioxidant capacity of serum together [45]. Convincing beneficial effects of a combination of vitamin E, vitamin C, and L-arginine, the natural precursor of NO, have been provided both on eNOS and oxidation-sensitive gene expression in human endothelial cells exposed to shear stress in vitro and in vivo [46].…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of EPA and Deleterious Effects of DHA on eNOS Activity in Ea hy 926 Cultured with Lysophosphatidylcholine

Tardivel

Gousset-Dupont

Robert

et al. 2009

Lipids

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Oxidized low density lipoprotein (Ox-LDL) is a well-established risk factor in atherosclerosis and lysophosphatidylcholine (LysoPtdCho) is considered to be one of the major atherogenic component of Ox-LDL. The purpose of this work was to investigate the effects of two membrane n-3 long chain polyunsaturated fatty acids (n-3 PUFAs), EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) compared to n-6 PUFA, ARA (arachidonic acid), on the activation of endothelial NO synthase (eNOS) by histamine in Ea hy 926 endothelial cells incubated during 24 h in the presence or the absence of LysoPtdCho. DHA (50 muM) produced a ROS induction in cells and aggravated the LysoPtdCho-induced oxidative stress. It did not modify the basal eNOS activity but impaired the stimulation of eNOS induced by histamine and was unable to correct the deleterious effect of LysoPtdCho on histamine-stimulated eNOS activity or phosphorylation of Ser 1177. In contrast, EPA (90 muM) did not modify the ROS level produced in the presence or absence of LysoPtdCho or basal eNOS activity and the stimulating effect of histamine on eNOS. However, it diminished the deleterious effect of LysoPtdCho as well as on the histamine-stimulated eNOS activity on the phosphorylation on Ser 1177 of eNOS. The beneficial effect of EPA but not DHA on endothelial eNOS activity in Ea hy 926 could be also partially due to a slight decrease in membrane DHA content in EPA-treated cells. Consequently, the equilibrium between NO generated by eNOS and ROS due to oxidative stress could explain, in part, the beneficial effect of EPA on the development of cardiovascular diseases. By contrast ARA an n-6 PUFA was devoid of any effect on ROS generation or eNOS activity in the basal state or after histamine-induced stimulation. In vivo experiments should be undertaken to confirm these results.

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Effects of combined dietary supplementation on oxidative and inflammatory status in dyslipidemic subjects

Cited by 56 publications

References 34 publications

Effect of marine n-3 fatty acids on circulating inflammatory markers in healthy subjects and subjects with cardiovascular risk factors

Effect of marine n-3 fatty acids on circulating inflammatory markers in healthy subjects and subjects with cardiovascular risk factors

Basic Mechanisms of Oxidative Stress and Reactive Oxygen Species in Cardiovascular Injury

Protective Effects of EPA and Deleterious Effects of DHA on eNOS Activity in Ea hy 926 Cultured with Lysophosphatidylcholine

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