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MiniReview |
-Tocopherol (Vitamin E)
From the Linus Pauling Institute, Oregon State University, Corvallis, Ore.
Correspondence to Balz Frei, PhD, Linus Pauling Institute, Oregon State University, 571 Weniger Hall, Corvallis, OR 97331-6512. E-mail balz.frei{at}orst.edu
AbstractThe premise that
oxidative stress, among several other factors, plays an important role
in atherogenesis implies that the development and progression of
atherosclerosis can be inhibited by antioxidants. In
this minireview we discuss several mechanisms by which the antioxidants
ascorbate (vitamin C) and
-tocopherol (vitamin E) may
protect against atherosclerosis. These mechanisms
include inhibition of LDL oxidation and inhibition of leukocyte
adhesion to the endothelium and vascular
endothelial dysfunction. Overall, ascorbate appears to
be more effective than
-tocopherol in mitigating these
pathophysiological processes, most likely as a
result of its abilities to effectively scavenge a wide range of
reactive oxygen and nitrogen species and to regenerate
-tocopherol, and possibly tetrahydrobiopterin, from its
radical species. In contrast,
-tocopherol can act either
as an antioxidant or a pro-oxidant to inhibit or facilitate,
respectively, lipid peroxidation in LDL. However, this pro-oxidant
activity of
-tocopherol is prevented by ascorbate acting
as a coantioxidant. Therefore, an optimum vitamin C intake or body
status may help protect against atherosclerosis and its
clinical sequelae, whereas vitamin E may only be effective in
combination with vitamin C.
Key Words: ascorbic acid atherosclerosis endothelial cells low-density lipoprotein vitamin E
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