Protective effect of vitamin E supplements on experimental atherosclerosis is modest and depends on preexisting vitamin E deficiency

Vitamin E has failed to protect humans from cardiovascular disease outcome, yet its role in experimental atherosclerosis remains less clear. A previous study ( Proc. Natl. Acad. Sci. USA 97:13830–13834; 2000) showed that vitamin E deficiency caused by disruption of the α-tocopherol transfer protein...

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Published in:Free radical biology & medicine 2006-09, Vol.41 (5), p.722-730
Main Authors: Suarna, Cacang, Wu, Ben J., Choy, Katherine, Mori, Trevor, Croft, Kevin, Cynshi, Osamu, Stocker, Roland
Format: Article
Language:English
Subjects:
alpha-Tocopherol - metabolism
Animals
Apolipoproteins E - genetics
Atherosclerosis - genetics
Atherosclerosis - metabolism
Atherosclerosis - therapy
Benzofurans - pharmacology
BO-653
Coenzyme Q
Dietary Supplements
Lipid oxidation
Lipid Peroxidation
Lipoproteins - metabolism
Male
Mice
Mice, Transgenic
Oxidative Stress
Oxygen - metabolism
Ubiquinone - pharmacology
Vitamin E - pharmacology
Vitamin E Deficiency
α-Tocopherol
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Summary:Vitamin E has failed to protect humans from cardiovascular disease outcome, yet its role in experimental atherosclerosis remains less clear. A previous study ( Proc. Natl. Acad. Sci. USA 97:13830–13834; 2000) showed that vitamin E deficiency caused by disruption of the α-tocopherol transfer protein gene ( Ttpa) is associated with a modest increase in atherosclerosis in apolipoprotein E gene deficient ( Apoe −/−) mice. Here we confirm this finding and report that in Apoe −/− Ttpa −/− mice dietary α-tocopherol (αT) supplements restored circulating and aortic levels of αT, and decreased atherosclerosis in the aortic root to a level comparable to that seen in Apoe −/− mice. However, such dietary supplements did not decrease disease in Apoe −/− mice, whereas dietary supplements with a synthetic vitamin E analog (BO-653), either alone or in combination with αT, decreased atherosclerosis in Apoe −/− and in Apoe −/− Ttpa −/− mice. Differences in atherosclerosis were not associated with changes in the arterial concentrations of F 2-isoprostanes and cholesterylester hydro(pero)xides, nor were they reflected in the resistance of plasma lipids to ex vivo oxidation. These results show that vitamin E at best has a modest effect on experimental atherosclerosis in hyperlipidemic mice, and only in situations of severe vitamin E deficiency and independent of lipid oxidation in the vessel wall.
ISSN:0891-5849
1873-4596
DOI:10.1016/j.freeradbiomed.2006.05.013