Health Implications of Vitamin E and Its Analogues and Metabolites

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 10 February 2027 | Viewed by 3701

Special Issue Editors


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Guest Editor
Department of Biochemistry and Molecular Biology, Miller School of Medicine, University of Miami, Miami, FL 33136, USA
Interests: vitamin E; curcumin; signal transduction; gene expression; senescence

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Guest Editor
Laboratory of Food Function Analysis, Graduate School of Agricultural Science, Tohoku University, Sendai 980-8577, Japan
Interests: food function; antioxidant; curcumin; lipid oxidation; oxidative stress
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Guest Editor
New Industry Creation Hatchery Center (NICHe), Tohoku University, Sendai 980-8579, Japan
Interests: curcumin; nanoparticles; redox regulation; surfactant; soft matter
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Special Issue Information

Dear Colleagues,

Several natural vitamin E analogues are present in plants in various amounts, but only one of them, RRR-α-tocopherol, is enriched during uptake from the diet and considered essential. The other vitamin E analogues are less bioavailable and considered nonessential but nevertheless can influence human and animal health by modulating signalling and gene expression in antioxidant and non-antioxidant manners. These activities of vitamin E analogues contribute to the preventive effects against several diseases that often have an inflammatory component, including cardiovascular, neurodegenerative, and liver diseases (e.g., Metabolic Dysfunction-Associated Steatohepatitis (MASH)).

In this Special Issue in the journal Antioxidants, the molecular mechanisms by which vitamin E and its analogues and metabolites may have an impact on disease prevention and human health are reviewed. The significance of vitamin E in food is also included in the scope.

Dr. Jean-Marc Zingg
Prof. Dr. Kiyotaka Nakagawa
Dr. Taiki Miyazawa
Guest Editors

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Keywords

  • vitamin E
  • antioxidant
  • non-antioxidant
  • bioavailability
  • bioactivity
  • signalling
  • gene expression

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Published Papers (1 paper)

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Research

24 pages, 2225 KB  
Article
Differential Regulatory Effects of Cannabinoids and Vitamin E Analogs on Cellular Lipid Homeostasis and Inflammation in Human Macrophages
by Mengrui Li, Sapna Deo, Sylvia Daunert and Jean-Marc Zingg
Antioxidants 2026, 15(1), 119; https://doi.org/10.3390/antiox15010119 - 16 Jan 2026
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Abstract
Cannabinoids can bind to several cannabinoid receptors and modulate cellular signaling and gene expression relevant to inflammation and lipid homeostasis. Likewise, several vitamin E analogs can modulate inflammatory signaling and foam cell formation in macrophages by antioxidant and non-antioxidant mechanisms. We analyzed the [...] Read more.
Cannabinoids can bind to several cannabinoid receptors and modulate cellular signaling and gene expression relevant to inflammation and lipid homeostasis. Likewise, several vitamin E analogs can modulate inflammatory signaling and foam cell formation in macrophages by antioxidant and non-antioxidant mechanisms. We analyzed the regulatory effects on the expression of genes involved in cellular lipid homeostasis (e.g., CD36/FAT cluster of differentiation/fatty acid transporter and scavenger receptor SR-B1) and inflammation (e.g., inflammatory cytokines, TNFα, IL1β) by cannabinoids (cannabidiol (CBD) and Δ9-tetrahydrocannabinol (THC)) in human THP-1 macrophages with/without co-treatment with natural alpha-tocopherol (RRR-αT), natural RRR-αTA (αTAn), and synthetic racemic all-rac-αTA (αTAr). In general, αTAr inhibited both lipid accumulation and the inflammatory response (TNFα, IL6, IL1β) more efficiently compared to αTAn. Our results suggest that induction of CD36/FAT mRNA expression after treatment with THC can be prevented, albeit incompletely, by αTA (either αTAn or αTAr) or CBD. A similar response pattern was observed with genes involved in lipid efflux (ABCA1, less with SR-B1), suggesting an imbalance between uptake, metabolism, and efflux of lipids/αTA, increasing macrophage foam cell formation. THC increased reactive oxygen species (ROS), and co-treatment with αTAn or αTAr only partially prevented this. To study the mechanisms by which inflammatory and lipid-related genes are modulated, HEK293 cells overexpressing cannabinoid receptors (CB1 or TRPV-1) were transfected with luciferase reporter plasmids containing the human CD36 promoter or response elements for transcription factors involved in its regulation (e.g., LXR and NFκB). In cells overexpressing CB1, we observed activation of NFκB by THC that was inhibited by αTAr. Full article
(This article belongs to the Special Issue Health Implications of Vitamin E and Its Analogues and Metabolites)
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