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Supplement

The Effect of -Tocopherol on Monocyte Proatherogenic Activity¹

Ishwarlal Jialal^*,2, Sridevi Devaraj^* and Nalini Kaul^*

Departments of ^* Pathology and Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390-9073

²To whom correspondence should be addressed. E-mail: jialal.i{at}pathology.swmed.edu

Atherosclerosis is the leading cause of morbidity and mortality in Westernized populations. The monocyte is a crucial cell in the genesis of the atherosclerotic lesion and is present during all stages of atherosclerosis. -Tocopherol (AT) is the most active component of the vitamin E family and is the principal and most potent lipid-soluble antioxidant in plasma and LDL. With regard to monocyte function, AT supplementation (1200 IU/d) has been shown to decrease release of reactive oxygen species, lipid oxidation, release of cytokines such as interleukin-1ß (IL-1ß) and tumor necrosis factor- (TNF-) and decrease adhesion of monocytes to human endothelium. The mechanism of inhibition of superoxide and lipid oxidation by monocytes appears to be via inhibition of protein kinase C (PKC), the decrease in IL-1ß and TNF- release by inhibition of 5-lipoxygenase and the inhibition of monocyte-endothelial cell adhesion via decrease in adhesion molecules on monocytes, CD11b and VLA-4 and by decreasing DNA-binding activity of nuclear transcription factor B. Thus, in addition to the decrease in oxidative stress resulting from AT supplementation, as evidenced by decreased F₂-isoprostanes and LDL oxidizability, AT is anti-inflammatory and exerts beneficial antiatherogenic effects on cells crucial in atherogenesis such as monocytes.

KEY WORDS: • -tocopherol • monocytes • vitamin E • inflammation • antioxidant

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