The effects of alpha tocopherol supplementation on monocyte function. Decreased lipid oxidation, interleukin 1 beta secretion, and monocyte adhesion to endothelium
Open accessAbstract
Low levels of alpha tocopherol are related to a higher incidence of cardiovascular disease and increased intake appears to afford protection against cardiovascular disease. In addition to decreasing LDL oxidation, alpha tocopherol may exert intracellular effects on cells crucial in atherogenesis, such as monocytes. Hence, the aim of this study was to test the effect of alpha tocopherol supplementation on monocyte function relevant to atherogenesis. Monocyte function was assessed in 21 healthy subjects at baseline, after 8 wk of supplementation with d-alpha tocopherol (1,200 IU/d) and after a 6-wk washout phase. The release of reactive oxygen species (superoxide anion, hydrogen peroxide), lipid oxidation, release of the potentially atherogenic cytokine, interleukin 1 beta, and monocyte-endothelial adhesion were studied in the resting state and after activation of the monocytes with lipopolysaccharide at 0, 8, and 14 wk. There was a 2.5-fold increase in plasma lipid-standardized and monocyte alpha tocopherol levels in the supplemented phase. After alpha tocopherol supplementation, there were significant decreases in release of reactive oxygen species, lipid oxidation, IL-1 beta secretion, and monocyte-endothelial cell adhesion, both in resting and activated cells compared with baseline and washout phases. Studies with the protein kinase C inhibitor, Calphostin C, suggest that the inhibition of reactive oxygen species release and lipid oxidation is due to an inhibition of protein kinase C activity by alpha tocopherol. Thus, this study provides novel evidence for an intracellular effect of alpha tocopherol in monocytes that is antiatherogenic.
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Vitamin D has several anti-inflammatory actions.
“Vitamin D has several anti-inflammatory actions.”
From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [731]
Vitamin D blunts the pro-inflammatory effects of advanced glycation end products on endothelial cells, suggesting it acts as an endogenous vascular protector against their deleterious effects.
“It blunts the pro-inflammatory effects of AGE on endothelial cells, suggesting that it acts as an endogenous vascular protector counteracting the possible deleterious effects of AGE (731) .”
From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [731]
Vitamin E has been shown to have anti-inflammatory properties.
“Vitamin E has been shown to have anti-inflammatory properties (Devaraj et al. 1996; Mandal et al. 2022)”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Devaraj et al. 1996
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References 70 · Cited by 333
- Authors
- Devaraj, S., Li, D., & Jialal, I.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- ORCID
- Jialal, I
- Venue
- Journal of Clinical Investigation
- Published
- 1996-08-01
- Volume
- 98
- Issue
- 3
- Pages
- 756-763
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC507486
- OpenAlex
- W2060845714
- Cited by
- 333
- References
- 70
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2023: 3 · 2022: 3 · 2021: 5 · 2020: 6 · 2019: 4 · 2018: 8 · 2017: 7 · 2016: 3 · 2015: 7 · 2014: 5 · 2013: 7 · 2012: 11
- FWCI
- 11.86
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Diabetes Association
- Topics
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
- Keywords
- alpha-tocopherol, vitamin E supplementation, monocytes, atherogenesis, lipid oxidation, IL-1β, monocyte-endothelial adhesion, reactive oxygen species, protein kinase C, calphostin C, lipopolysaccharide stimulation, cardiovascular disease prevention
- MeSH terms
- Adult, Arteriosclerosis, Cell Adhesion, Endothelium, Vascular, Humans, Interleukin-1, Lipopolysaccharides, Lipoproteins, LDL, Monocytes, Oxidation-Reduction, Superoxides, Vitamin E
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