The role of vitamin E (tocopherol) supplementation in the prevention of stroke

Bin, Qiong; Hu, Xiaofang; Cao, Yukun; Gao, Feng

doi:10.1160/th10-11-0729

Cited by 52 publications

(44 citation statements)

References 37 publications

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“…95% CI, 0.94 -1.09), or hemorrhagic stroke (RR, 1.12; 95% CI, 0.94 -1.33). 16 There was no significant heterogeneity among the trials (P for heterogeneityϭ0.37). The results were consistent irrespective of vitamin E source (natural versus synthetic), vitamin E dose (Ͻ or Ͼ200 IU/day), and baseline health status.…”

Section: Vitamin Ementioning

confidence: 93%

Vitamin Supplementation and Stroke Prevention

Hankey

2012

Stroke

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Section: Vitamin Ementioning

confidence: 93%

Vitamin Supplementation and Stroke Prevention

Hankey

2012

Stroke

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“…• exerts pleiotropic antithrombotic effects by (1) increasing sGC-derived cGMP to decrease the [Ca 2+ ]i flux that is required for activation of the platelet aggregation molecule glycoprotein IIb/IIIa, 56 (2) inhibiting thrombin, 57 (3) increasing synthesis of prostacyclin 58 and (4) increasing cAMP levels to induce phospholamban phosphorylation-mediated decreases in [Ca 2+ ]i 59 (Figure 4). NO • may also indirectly influence blood vessel tone by functioning as an antioxidant inhibiting the effects of ROS on vasodilatory cell signaling pathways; for example, through NO • -mediated upregulation heme-oxygenase-I (see later section on antioxidant enzymes) and SOD.…”

Section: Nomentioning

confidence: 99%

“…Although some clinical trials have found beneficial effects of these, metaanalyses of numerous clinical trials have found no net benefit, and there may possibly be detrimental effects of nonspecific antioxidant therapies. 2 These unsuccessful clinical efforts to use antioxidant vitamins or dietary supplements to prevent or ameliorate the detrimental effects of increased vascular oxidant stress in humans have led to a resurgence of investigations that aim to define with greater specificity the precise mechanism(s) by which oxygen free radicals promote vascular diseases. 3- 7 The recognition of physiological roles for reactive oxygen species (ROS) such as hydrogen peroxide (H2O2) may indicate that the broad use of nonspecific antioxidant supplements may interfere with normal cellular responses and could undermine any possible health benefit that might theoretically derive from a decrease in oxidative stress.…”

mentioning

confidence: 99%

Subcellular Localization of Oxidants and Redox Modulation of Endothelial Nitric Oxide Synthase

Maron

Michel

2012

Circ J

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Reactive oxygen species (ROS) have long been viewed as deleterious chemicals that lead to oxidative stress. More recently, ROS, especially the stable ROS hydrogen peroxide (H2O2), have been shown to have roles in normal physiological responses in vascular cells. Endothelial nitric oxide synthase (eNOS) is dynamically targeted to plasmalemmal caveolae, and represents the principal enzymatic source of nitric oxide (NO • ) in the vascular wall. eNOS maintains normal vascular tone and inhibits the clinical expression of many cardiovascular diseases. Increases in oxidative stress are associated with eNOS dysfunction. In a paradigm shift in the conceptual framework linking redox biochemistry and vascular function, H2O2 has been established as a physiological mediator in signaling pathways, yet the intracellular sources of H2O2 and their regulation remain incompletely understood. The subcellular distributions of ROS and of ROS-modified proteins critically influence the redox-sensitive regulation of eNOS-dependent pathways. ROS localization in specific subcellular compartments can lead to selective oxidative modifications of eNOS and eNOS-associated proteins. Likewise, the dynamic targeting of eNOS and other signaling proteins influences their interactions with reactive nitrogen species and ROS that are also differentially distributed within the cell. Thus, the subcellular distribution both of eNOS and redox-active biomolecules serves as a critical basis for the control of the "redox switch" that influences NO• - and oxidant-regulated signaling pathways. Here we discuss the biochemical factors, cellular determinants, and molecular mechanisms that modulate redox-sensitive regulation of eNOS and NO tion of eNOS is dynamically regulated 9 and the enzyme is thus exposed to different concentrations of ROS depending upon where in the cell the protein is localized. Alterations in eNOS function due to changes in ROS levels may reflect either physiological or pathological responses in both normal cells and in vascular disease states. The relationship between impaired eNOS activity and the development of vascular dysfunction has been extensively studied: NO • is a potent vasodilator molecule that also attenuates platelet aggregation, vascular smooth muscle cell (VSMC) proliferation, and negative vascular remodeling. 10 Collectively, these properties contribute to the prevention of intermediate pathophenotypes of vascular disease, including cardiac and/or vascular hypertrophy, fibrosis, and atherosclerosis. In counterpoise to these deleterious effects of ROS, there also appears to be a key physiological role for H2O2 in eNOS regulation. 11 Elucidating the redoxdependent mechanisms involved in the physiological and pathophysiological regulation of eNOS by ROS will provide critical new insights into vascular disease states and may lead to the identification of novel treatment targets related to eNOS and eNOS-modulated vascular responses.

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“…It is known that patients with CKD have reduced levels of tocopherol in plasma, which is a prerequisite for this use in therapies [13]. Previous studies have shown that administration of tocopherol in patients with CKD helped to reduce the risk of cardiovascular complications, increased activity of endogenous antioxidant systems -GPX, catalase [14].…”

Section: Discussionmentioning

confidence: 99%

Possible therapeutic approach to apoptosis correction in nephrotic children

Burlaka¹

2017

Clin Diagn Pathol

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Objectives: the objective of this paper was to study the levels of apoptosis controlling factors and nuclear transcriptional factor NF-κB in relation to the value of kidney function impairment; to evaluate possible protective effects of conventional therapy with addition of antioxidant agent tocopherol in pediatric patients with nephrotic syndrome.Background: hypoxia-related disorders play an important role in irreversible kidney tissue damage via activation of certain secondary processes, i.e. apoptosis.

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The role of vitamin E (tocopherol) supplementation in the prevention of stroke

Cited by 52 publications

References 37 publications

Vitamin Supplementation and Stroke Prevention

Vitamin Supplementation and Stroke Prevention

Subcellular Localization of Oxidants and Redox Modulation of Endothelial Nitric Oxide Synthase

Possible therapeutic approach to apoptosis correction in nephrotic children

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