scholarly journals Vitamin E Metabolic Effects and Genetic Variants: A Challenge for Precision Nutrition in Obesity and Associated Disturbances

Nutrients ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 1919 ◽  
Author(s):  
Sebastià Galmés ◽  
Francisca Serra ◽  
Andreu Palou
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Genetic Variants ◽  
Metabolic Effects ◽  
Dietary Recommendations ◽  
The Core ◽  
Leading Role ◽  
Dietary Reference Values ◽  
Per Se

Vitamin E (VE) has a recognized leading role as a contributor to the protection of cell constituents from oxidative damage. However, evidence suggests that the health benefits of VE go far beyond that of an antioxidant acting in lipophilic environments. In humans, VE is channeled toward pathways dealing with lipoproteins and cholesterol, underlining its relevance in lipid handling and metabolism. In this context, both VE intake and status may be relevant in physiopathological conditions associated with disturbances in lipid metabolism or concomitant with oxidative stress, such as obesity. However, dietary reference values for VE in obese populations have not yet been defined, and VE supplementation trials show contradictory results. Therefore, a better understanding of the role of genetic variants in genes involved in VE metabolism may be crucial to exert dietary recommendations with a higher degree of precision. In particular, genetic variability should be taken into account in targets concerning VE bioavailability per se or concomitant with impaired lipoprotein transport. Genetic variants associated with impaired VE liver balance, and the handling/resolution of oxidative stress might also be relevant, but the core information that exists at present is insufficient to deliver precise recommendations.

Association between alcohol-induced oxidative stress and membrane properties in synaptosomes: A protective role of vitamin E

2017 ◽  
Vol 63 ◽  
pp. 60-65 ◽  
Author(s):  
Vaddi Damodara Reddy ◽  
Pannuru Padmavathi ◽  
Saradamma Bulle ◽  
Ananda Vardhan Hebbani ◽  
Shakeela Begum Marthadu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Protective Role ◽  
Membrane Properties

scholarly journals Vitamin E Analogues Inhibit Angiogenesis by Selective Induction of Apoptosis in Proliferating Endothelial Cells: The Role of Oxidative Stress

2007 ◽  
Vol 67 (24) ◽  
pp. 11906-11913 ◽  
Author(s):  
L.-F. Dong ◽  
E. Swettenham ◽  
J. Eliasson ◽  
X.-F. Wang ◽  
M. Gold ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Vitamin E ◽  
Induction Of Apoptosis

Role of vitamin E and oxidative stress in exercise

Nutrition ◽  
2001 ◽  
Vol 17 (10) ◽  
pp. 809-814 ◽  
Author(s):  
Jennifer M. Sacheck ◽  
Jeffrey B. Blumberg
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
And Oxidative Stress

scholarly journals Putative role of pharmacogenetics to elucidate the mechanism of tardive dyskinesia in schizophrenia

2019 ◽  
Vol 20 (17) ◽  
pp. 1199-1223 ◽  
Author(s):  
Anton JM Loonen ◽  
Bob Wilffert ◽  
Svetlana A Ivanova
Keyword(s):  
Oxidative Stress ◽  
Tardive Dyskinesia ◽  
Genetic Variants ◽  
Long Term Potentiation ◽  
Specific Gene ◽  
Medium Spiny Neurons ◽  
Spiny Neurons ◽  
Long Term Treatment

Identifying biomarkers which can be used as a diagnostic tool is a major objective of pharmacogenetic studies. Most mental and many neurological disorders have a compiled multifaceted nature, which may be the reason why this endeavor has hitherto not been very successful. This is also true for tardive dyskinesia (TD), an involuntary movement complication of long-term treatment with antipsychotic drugs. The observed associations of specific gene variants with the prevalence and severity of a disorder can also be applied to try to elucidate the pathogenesis of the condition. In this paper, this strategy is used by combining pharmacogenetic knowledge with theories on the possible role of a dysfunction of specific cellular elements of neostriatal parts of the (dorsal) extrapyramidal circuits: various glutamatergic terminals, medium spiny neurons, striatal interneurons and ascending monoaminergic fibers. A peculiar finding is that genetic variants which would be expected to increase the neostriatal dopamine concentration are not associated with the prevalence and severity of TD. Moreover, modifying the sensitivity to glutamatergic long-term potentiation (and excitotoxicity) shows a relationship with levodopa-induced dyskinesia, but not with TD. Contrasting this, TD is associated with genetic variants that modify vulnerability to oxidative stress. Reducing the oxidative stress burden of medium spiny neurons may also be the mechanism behind the protective influence of 5-HT2 receptor antagonists. It is probably worthwhile to discriminate between neostriatal matrix and striosomal compartments when studying the mechanism of TD and between orofacial and limb-truncal components in epidemiological studies.

Paradigm Function Morphology: Assumptions and Innovations

2020 ◽  
Author(s):  
Gregory Stump
Keyword(s):  
Inflectional Morphology ◽  
Formal Representation ◽  
The Core ◽  
Recent Innovation ◽  
Morphological Theory ◽  
Per Se ◽  
Fundamental Insight ◽  
Definition Of

Paradigm Function Morphology (PFM) is an evolving approach to modeling morphological systems in a precise and enlightening way. The fundamental insight of PFM is that words have both content and form and that in the context of an appropriately organized lexicon, a language’s morphology deduces a complex word’s form from its content. PFM is therefore a realizational theory: a language’s grammar and lexicon are assumed to provide a precise characterization of a word’s content, from which the language’s morphology then projects the corresponding form. Morphemes per se have no role in this theory; by contrast, paradigms have the essential role of defining the content that is realized by a language’s morphology. At the core of PFM is the notion of a paradigm function, a formal representation of the relation between a word’s content and its form; the definition of a language’s paradigm function is therefore the definition of its inflectional morphology. Recent elaborations of this idea assume a distinction between content paradigms and form paradigms, which makes it possible to account for a fact that is otherwise irreconcilable with current morphological theory—the fact that the set of morphosyntactic properties that determines a word’s syntax and semantics often differs from the set of properties (some of them morphomic) that determines a word’s inflectional form. Another recent innovation is the assumption that affixes and rules of morphology may be complex in the sense that they may be factored into smaller affixes and rules; the evidence favoring this assumption is manifold.

scholarly journals Role of Anti-oxidants in the Treatment of Vitiligo

2019 ◽  
Vol 17 (1) ◽  
pp. 49-57
Author(s):  
Amit Kumar ◽  
Sudha Agrawal ◽  
Tapan Kumar Dhali ◽  
Shankar Kumr Majhi
Keyword(s):  
Oxidative Stress ◽  
Placebo Group ◽  
Vitamin E ◽  
Primary Outcome ◽  
Antioxidant Supplementation ◽  
Significant Difference ◽  
Anti Oxidant ◽  
And Oxidative Stress

Introduction: The role of free radicals and oxidative damage in the pathophysiology of vitiligo has been documented in recent studies. Antioxidant supplementation has been reported to be useful in the treatment of vitiligo. Objective: To evaluate the role of oral antioxidants supplementation therapy in the treatment of vitiligo by assessing the onset of repigmentation and oxidative stress. Materials and Methods: A total of 80 cases of vitiligo randomized into two groups: antioxidant and placebo comprising 40 patients each and were followed up for 8 weeks for the assessment of onset of repigmentation of vitiliginous lesions as primary outcome.  The activities of Malondialdehyde (MDA), Vitamin C, and Vitamin E in serum and of Catalase (CAT) in erythrocytes of patients at baseline and at end of eight weeks were also assessed by using the spectrophotometric assay. Results: The onset of repigmentation was noted significantly earlier among the anti-oxidant group as compared to the placebo group (p=0.015). At the baseline, between the two groups, no significant difference was found in the different biochemical parameters. However, at the end of 2 months the level of MDA (p<0.001) was found to be significantly lower and that of Vitamin E (p<0.001) and CAT (p=0.005) was significantly higher among the anti-oxidants group as compared to the placebo group. Conclusion: Antioxidant supplementation carried a better response in terms of early onset of repigmentation and significant decrease in the oxidative stress, in the short follow up of two months.

scholarly journals The Role of Oxidative Stress in Parkinson’s Disease

Antioxidants ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 597 ◽  
Author(s):  
Kuo-Hsuan Chang ◽  
Chiung-Mei Chen
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Vitamin E ◽  
Coenzyme Q10 ◽  
Conclusive Evidence ◽  
Abnormal Accumulation ◽  
Progressive Neurodegeneration ◽  
Antioxidative Treatment

Parkinson’s disease (PD) is caused by progressive neurodegeneration of dopaminergic (DAergic) neurons with abnormal accumulation of α-synuclein in substantia nigra (SN). Studies have suggested the potential involvement of dopamine, iron, calcium, mitochondria and neuroinflammation in contributing to overwhelmed oxidative stress and neurodegeneration in PD. Function studies on PD-causative mutations of SNCA, PRKN, PINK1, DJ-1, LRRK2, FBXO7 and ATP13A2 further indicate the role of oxidative stress in the pathogenesis of PD. Therefore, it is reasonable that molecules involved in oxidative stress, such as DJ-1, coenzyme Q10, uric acid, 8-hydroxy-2’-deoxyguanosin, homocysteine, retinoic acid/carotenes, vitamin E, glutathione peroxidase, superoxide dismutase, xanthine oxidase and products of lipid peroxidation, could be candidate biomarkers for PD. Applications of antioxidants to modulate oxidative stress could be a strategy in treating PD. Although a number of antioxidants, such as creatine, vitamin E, coenzyme Q10, pioglitazone, melatonin and desferrioxamine, have been tested in clinical trials, none of them have demonstrated conclusive evidence to ameliorate the neurodegeneration in PD patients. Difficulties in clinical studies may be caused by the long-standing progression of neurodegeneration, lack of biomarkers for premotor stage of PD and inadequate drug delivery across blood–brain barrier. Solutions for these challenges will be warranted for future studies with novel antioxidative treatment in PD patients.

scholarly journals Cytoprotective role of vitamin E in porcine adipose-tissue-derived mesenchymal stem cells against hydrogen-peroxide-induced oxidative stress

2018 ◽  
Vol 374 (1) ◽  
pp. 111-120 ◽  
Author(s):  
Fazal Ur Rehman Bhatti ◽  
Song Ja Kim ◽  
Ae-Kyung Yi ◽  
Karen A. Hasty ◽  
Hongsik Cho
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Adipose Tissue ◽  
Vitamin E
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