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Senior Nutrition, Vitamins, Supplements
Vitamin E Offshoot Transformed to Potent Cancer
Killer
'Such an agent might help reduce the risk of
prostate, colon and other cancers'
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Ching-Shih Chen
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May 20, 2006 - Researchers have learned how a
derivative of vitamin E causes the death of cancer cells and have used
this knowledge to make the agent an even more potent cancer killer.
The compound, called
vitamin E succinate, or
alpha tocopheryl succinate, is taken by some people as a nutritional
supplement, mainly for its antioxidant properties. In addition, it has a
weak ability to kill cancer cells, and it has been tested as a cancer
chemopreventive agent.
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on
Nutrition, Vitamins & Supplements |
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The substance kills cancer cells by causing them to
undergo a natural process known as programmed cell death, or apoptosis.
Until now, no one knew how the agent caused this to happen.
These findings answer that question and also
indicate that the molecule's antitumor activity is separate from its
antioxidant effect.
The study, led by researchers with
The Ohio State University Comprehensive Cancer Center
Arthur G. James Cancer Hospital and Richard J. Solove Research Institute
(OSUCCC-James), is published in the April 28 issue of the
Journal of Biological Chemistry.
Our findings could lead to a potent
chemopreventive agent that has both strong anticancer and antioxidant
properties, says principal investigator
Ching-Shih Chen, professor of
pharmacy and of
internal medicine and a researcher with the OSUCCC-James.
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The scientists found that a
relatively simple process of altering the molecule's structure
basically cutting the tail short allowed a tighter fit and
improved the agent's ability to kill cancer cells by five- to
ten-fold in laboratory tests.
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Such an agent might help reduce the risk of
prostate, colon and other cancers.
Chen and his collaborators found that vitamin E
succinate works by blocking a protein called Bcl-xL. The protein, which
is made by healthy cells, is often present at abnormally high levels in
cancer cells and protects them from dying when they should.
Using computer modeling, the researchers found that
the vitamin E derivative works because it lodges in a groove in the
structure of the Bcl-xL protein, disabling it.
However, the vitamin E molecule has a long, coiled,
protruding tail that keeps the molecule from fitting tightly, and more
effectively, into the groove.
Once we identified how the agent and the protein
interact, we asked how we could improve that interaction, Chen says.
The scientists found that a relatively simple
process of altering the molecule's structure basically cutting the
tail short allowed a tighter fit and improved the agent's ability to
kill cancer cells by five- to ten-fold in laboratory tests.
Overall, out findings are proof of the principle
that this drug can kill cancer cells very effectively but does very
little damage to healthy cells, Chen says.
Chen is also the Lucius A. Wing chair of cancer
research and therapy at the OSUCCC-James and the Kimberly professor of
pharmacy
Funding from the
National Cancer Institute supported this research.
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Learn More About Vitamin E |
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A large and growing body of
experimental evidence suggests that high intakes of vitamin
E may lower the risk of some chronic diseases, especially
heart disease. However, the limited and discordant clinical
trial evidence available precludes recommendations at this
time of higher vitamin E intakes to reduce chronic disease
risk. The Tolerable Upper Intake Level (UL) for adults is
set at 1,000 mg (2,325 ΅mol)/day of any form of supplemental
α-tocopherol based on the adverse effect of increased
tendency to hemorrhage.
"Dietary
Reference Intakes for Vitamin C, Vitamin E, Selenium, and
Carotenoids (2000)" - Institute of Medicine
More about Vitamin E
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