We use cookies to understand how you use our site and to improve your experience. This includes personalizing content and advertising. To learn more, click here. By continuing to use our site, you accept our use of cookies. Cookie Policy.

Features Partner Sites Information LinkXpress hp
Sign In
Advertise with Us

Download Mobile App




Events

19 May 2026 - 22 May 2026
17 Jun 2026 - 19 Jun 2026

Vitamin E Derivative May Kill Cancer

By HospiMedica staff writers
Posted on 02 Jun 2006
Researchers have discovered how an offshoot of vitamin E causes the death of cancer cells. More...
They then used that knowledge to make the agent an even more effective cancer killer.

The compound, called vitamin E succinate, or alpha tocopheryl succinate, is taken by some individuals as a nutritional supplement, mainly for its antioxidant characteristics. Furthermore, it has a weak ability to kill cancer cells, and it has been evaluated as a cancer chemopreventive agent. The substance kills cancer cells by causing them to undergo a natural process known as programmed cell death, or apoptosis. Up to now, no one knew how the agent caused this to occur. These new 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 (OSU; Columbus, OH, USA) Comprehensive Cancer Center--Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC-James), is published in the April 28, 2006, issue of the Journal of Biological Chemistry.

"Our findings could lead to a potent chemopreventive agent that has both strong anticancer and antioxidant properties,” commented lead investigator Dr. Ching-Shih Chen, professor of pharmacy and of internal medicine and a researcher with the OSUCCC-James. "Such an agent might help reduce the risk of prostate, colon and other cancers.”

Dr. Chen and coworkers discovered that vitamin E succinate functions by blocking a protein called Bcl-xL. The protein, which is made by healthy cells, is frequently present at abnormally high levels in cancer cells and protects them from dying when they should. Utilizing computer modeling, the investigators found that the vitamin E derivative works because it lodges in a groove in the structure of the Bcl-xL protein, disarming it.

However, the vitamin E molecule has a long, coiled, tail that juts out and 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,” stated Dr. Chen.

The scientists found that a relatively simple process of changing 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 10-fold in laboratory tests. "Overall, our findings are proof of the principle that this drug can kill cancer cells very effectively but does very little damage to healthy cells,” Dr. Chen said.



Related Links:
Ohio State University

New
Gold Member
Handheld Blood Glucose Analyzer
STAT-Site
Gold Member
STI Test
Vivalytic Sexually Transmitted Infection (STI) Array
New
Patient Monitoring System
AlarmSense
New
POC Respiratory/Sore Throat Test
BIOFIRE SPOTFIRE (R/ST) Panel
Read the full article by registering today, it's FREE! It's Free!
Register now for FREE to HospiMedica.com and get access to news and events that shape the world of Hospital Medicine.
  • Free digital version edition of HospiMedica International sent by email on regular basis
  • Free print version of HospiMedica International magazine (available only outside USA and Canada).
  • Free and unlimited access to back issues of HospiMedica International in digital format
  • Free HospiMedica International Newsletter sent every week containing the latest news
  • Free breaking news sent via email
  • Free access to Events Calendar
  • Free access to LinkXpress new product services
  • REGISTRATION IS FREE AND EASY!
Click here to Register








Channels

Copyright © 2000-2026 Globetech Media. All rights reserved.