Omega-3 Polyunsaturated Fatty Acids Protect against Cigarette Smoke-Induced Oxidative Stress and Vascular Dysfunction

Wiest, E; Walsh-Wilcox, Mary T.; Walker, Mary

doi:10.1093/toxsci/kfw255

Cited by 29 publications

(27 citation statements)

References 70 publications

(71 reference statements)

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“…thelial dysfunction is compromised in smokers. FMD can be considered a predictor marker for future cardiovascular events and that smoking cessation can improve this parameter [59].…”

Section: Wiest Et Al Demonstrated That Flow-mediated Dilation (Fmd) mentioning

confidence: 99%

Effects of Smoking on Oxidative Stress and Vascular Function

Carnevale¹,

Cammisotto²,

Pagano³

et al. 2018

Smoking Prevention and Cessation

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Tobacco smoking is the single most preventable risk factor related to the development of cardiovascular disease. It was demonstrated that tobacco smoke contains a thousand compounds potentially harmful to human health. As tobacco use declined over time, electronic cigarettes were introduced as an alternative. E-cigarettes are a modern and technological surrogate of traditional cigarettes and use heat to convert a nicotine solution or a flavored nicotine-free solution into vapor. Even though all the ingredients contained in the liquid of E-cigarettes are approved as food additives, the harmlessness of these electronic devices is still not fully proven in humans. The general mechanisms by which smoking results in cardiovascular events include the development of atherosclerotic changes with a hypercoagulable state and an increased risk of thrombosis. Endothelial dysfunction has been recognized as a hallmark of preclinical systemic atherosclerosis and as a useful marker to stratify the risk of cardiovascular disease. Based on these considerations, in this chapter, we (1) discussed the role of endothelial dysfunction and its contributing factors, such as oxidative stress and inflammation, in the development of cardiovascular diseases and (2) reported the studies which investigated the effect of tobacco and electronic smoking on the biomarkers of endothelial dysfunction, oxidative stress, and inflammation.

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“…thelial dysfunction is compromised in smokers. FMD can be considered a predictor marker for future cardiovascular events and that smoking cessation can improve this parameter [59].…”

Section: Wiest Et Al Demonstrated That Flow-mediated Dilation (Fmd) mentioning

confidence: 99%

Effects of Smoking on Oxidative Stress and Vascular Function

Carnevale¹,

Cammisotto²,

Pagano³

et al. 2018

Smoking Prevention and Cessation

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“…The mixture of EPA and DHA suppresses the pro-inflammatory response in LPS-stimulated mouse microglia by activating deacetylase sirtuin1 [ 17 ]. In a mouse model of cigarette smoke (CS)-induced endothelial dysfunction, n-3 PUFA-enriched diet decreased CS-induced production of an oxidative stress marker, 8-isoprostane and significantly reduced the mRNA level of cytochrome P4501A1 [ 18 ]. Additionally, n-3 PUFA-enriched diet protected mice from Concanavalin A-induced liver injury and suppressed the expression of pro-inflammatory cytokines [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

Docosahexaenoic Acid Induces Expression of Heme Oxygenase-1 and NAD(P)H:quinone Oxidoreductase through Activation of Nrf2 in Human Mammary Epithelial Cells

et al. 2017

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Docosahexaenoic acid (DHA), an ω-3 fatty acid abundant in fish oils, has diverse health beneficial effects, such as anti-oxidative, anti-inflammatory, neuroprotective, and chemopreventive activities. In this study, we found that DHA induced expression of two representative antioxidant/cytoprotective enzymes, heme oxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase (NQO1), in human mammary epithealial (MCF-10A) cells. DHA-induced upregulation of these enzymes was accompanied by enhanced translocation of the redox-sensitive transcription factor Nrf2 into the nucleus and its binding to antioxidant response element. Nrf2 gene silencing by siRNA abolished the DHA-induced expression of HO-1 and NQO1 proteins. When MCF-10A cells were transfected with mutant constructs in which the cysteine 151 or 288 residue of Keap1 was replaced by serine, DHA-induced expression of HO-1 and NQO1 was markedly reduced. Moreover, DHA activated protein kinase C (PKC)δ and induced Nrf2 phosphorylation. DHA-induced phosphorylation of Nrf2 was abrogated by the pharmacological PKCδ inhibitor rottlerin or siRNA knockdown of its gene expression. The antioxidants N-acetyl-l-cysteine and Trolox attenuated DHA-induced activation of PKCδ, phosphorylation of Nrf2, and and its target protein expression. In conclusion, DHA activates Nrf2, possibly through modification of critical Keap1 cysteine 288 residue and PKCδ-mediated phosphorylation of Nrf2, leading to upregulation of HO-1 and NQO1 expression.

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Section: N-3 Pufasmentioning

confidence: 99%

“…Several reviews and meta-analyses have highlighted significant and relatively large improvements in endothelial function following supplementation with EPA or DHA as measured by flow-mediated dilation [571][572][573]. The fact that this benefit would appear to apply to individuals with a high risk of developing CVD and individuals whose risk of developing such a disease appears to be normal or low is encouraging [571][572][573]. Data suggesting that dietary supplementation with EPA and/or DHA improves platelet function and decreases PA in low-and high-risk individuals also suggests that PUFA supplementation may be of value in addressing high CVD risk in patients with neuroprogressive illnesses [574,575], reviewed in [576].…”

Section: N-3 Pufasmentioning

confidence: 99%

Endothelial dysfunction in neuroprogressive disorders—causes and suggested treatments

Morris

Puri²,

Olive

et al. 2020

BMC Med

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Background Potential routes whereby systemic inflammation, oxidative stress and mitochondrial dysfunction may drive the development of endothelial dysfunction and atherosclerosis, even in an environment of low cholesterol, are examined. Main text Key molecular players involved in the regulation of endothelial cell function are described, including PECAM-1, VE-cadherin, VEGFRs, SFK, Rho GEF TRIO, RAC-1, ITAM, SHP-2, MAPK/ERK, STAT-3, NF-κB, PI3K/AKT, eNOS, nitric oxide, miRNAs, KLF-4 and KLF-2. The key roles of platelet activation, xanthene oxidase and myeloperoxidase in the genesis of endothelial cell dysfunction and activation are detailed. The following roles of circulating reactive oxygen species (ROS), reactive nitrogen species and pro-inflammatory cytokines in the development of endothelial cell dysfunction are then described: paracrine signalling by circulating hydrogen peroxide, inhibition of eNOS and increased levels of mitochondrial ROS, including compromised mitochondrial dynamics, loss of calcium ion homeostasis and inactivation of SIRT-1-mediated signalling pathways. Next, loss of cellular redox homeostasis is considered, including further aspects of the roles of hydrogen peroxide signalling, the pathological consequences of elevated NF-κB, compromised S-nitrosylation and the development of hypernitrosylation and increased transcription of atherogenic miRNAs. These molecular aspects are then applied to neuroprogressive disorders by considering the following potential generators of endothelial dysfunction and activation in major depressive disorder, bipolar disorder and schizophrenia: NF-κB; platelet activation; atherogenic miRs; myeloperoxidase; xanthene oxidase and uric acid; and inflammation, oxidative stress, nitrosative stress and mitochondrial dysfunction. Conclusions Finally, on the basis of the above molecular mechanisms, details are given of potential treatment options for mitigating endothelial cell dysfunction and activation in neuroprogressive disorders.

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Omega-3 Polyunsaturated Fatty Acids Protect against Cigarette Smoke-Induced Oxidative Stress and Vascular Dysfunction

Cited by 29 publications

References 70 publications

Effects of Smoking on Oxidative Stress and Vascular Function

Effects of Smoking on Oxidative Stress and Vascular Function

Docosahexaenoic Acid Induces Expression of Heme Oxygenase-1 and NAD(P)H:quinone Oxidoreductase through Activation of Nrf2 in Human Mammary Epithelial Cells

Endothelial dysfunction in neuroprogressive disorders—causes and suggested treatments

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