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Citations to this article

The effects of alpha tocopherol supplementation on monocyte function. Decreased lipid oxidation, interleukin 1 beta secretion, and monocyte adhesion to endothelium.
S Devaraj, … , D Li, I Jialal
S Devaraj, … , D Li, I Jialal
Published August 1, 1996
Citation Information: J Clin Invest. 1996;98(3):756-763. https://doi.org/10.1172/JCI118848.
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Research Article Article has an altmetric score of 6

The effects of alpha tocopherol supplementation on monocyte function. Decreased lipid oxidation, interleukin 1 beta secretion, and monocyte adhesion to endothelium.

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Abstract

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.

Authors

S Devaraj, D Li, I Jialal

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Citations to this article in year 2012 (8)

Title and authors Publication Year
The Anti-Inflammatory Role of Vitamin E in Prevention of Osteoporosis
AS Nazrun, M Norazlina, M Norliza, SI Nirwana
Advances in pharmacological sciences 2012
Evaluation of vitamin E in the treatment of erectile dysfunction in aged rats
MM Helmy, AM Senbel
Life Sciences 2012
HIV-1, reactive oxygen species, and vascular complications
KM Porter, RL Sutliff
Free radical biology & medicine 2012
L-Ascorbic Acid and Alpha-tocopherol Attenuates Liver Ischemia-Reperfusion Induced of Cardiac Function Impairment
CC Hsu, JJ Wang
Transplantation Proceedings 2012
A metabolomic investigation of the effects of vitamin E supplementation in humans
M Wong, JK Lodge
Nutrition & Metabolism 2012
Vitamins E and C Alleviate the Germ Cell Loss and Oxidative Stress in Cryptorchidism When Administered Separately but Not When Combined in Rats
AO Afolabi, OO Olotu, IA Alagbonsi
ISRN Pharmacology 2012
Vitamin E Isoforms Differentially Regulate Intercellular Adhesion Molecule-1 Activation of PKCα in Human Microvascular Endothelial Cells
H Abdala-Valencia, S Berdnikovs, JM Cook-Mills, L Buday
PloS one 2012
Non-Antioxidant Properties of α-Tocopherol Reduce the Anticancer Activity of Several Protein Kinase Inhibitors In Vitro
S Pédeboscq, C Rey, M Petit, C Harpey, FD Giorgi, F Ichas, L Lartigue, RP Singh
PloS one 2012

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