Written by Greg Arnold, DC, CSCS. In this cell study, exposure to vitamin E protected the cells 45% better than in the placebo group.
Vitamin E was first discovered in 1922. It was named tocopherol, from the Greek word “tokos” meaning childbirth (because it supported fertility), “phero” meaning to bring forth, and “ol” to indicate the alcohol properties of vitamin E. As an essential, fat soluble vitamin, vitamin E functions as an antioxidant in the human body. There are two types of vitamin E: tocopherols and tocotrienols, each of which has four different forms (alpha, beta, gamma, delta), giving a total of eight different forms called isomers.
Research over the past decade has shown that vitamin E tocotrienols very effectively help protect nerve health (1, 2, 3), especially after a stroke. There are 700,000 new stroke cases each year, and it is the third leading cause of death in the U.S. behind cancer and heart disease. However, it causes more serious long-term disabilities than any other disease. Nearly three out of every four strokes occur in people over the age of 65. For each decade after the age of 55, your risk of stroke doubles (4).
Now a new study (5) has suggested how vitamin E helps protect nerve health in nerve-damaging diseases like stroke. It was found to be so effective that this nerve-protecting property is “the most potent of all biological functions exhibited by any natural vitamin E molecule”.
In the study, researchers looked at vitamin E’s ability to control activity of a protein called PLA2, known to be “an important player” in the regulation of normal cell function of the central nervous system (6). They obtained tissue samples from pigs (called HT4 cells) and initially exposed them to a placebo or an amino acid called glutamate. This protein increases PLA2 activity and results in the release of a fat called arachidonic acid, signifying an early event along the “death pathway” of nerve cells. Compared to placebo, levels of arachidonic acid were 10 times higher in the glutamate-exposed cells, indicating high levels of PLA2 activity caused by glutamate.
The researchers then took the glutamate-exposed cells and exposed them to vitamin E tocotrienols (250 nanomolar). The researchers noted that vitamin E “significantly” inhibited arachidonic acid release from cells compared to the same in cells treated with glutamate alone. Specifically, arachidonic acid levels in the vitamin E cells were 45% lower than the glutamate group without vitamin E.
For the researchers, “This work presents first evidence recognizing glutamate-induced changes in cPLA2 as a [new] mechanism responsible for [nerve protection] observed in response to nanomolar concentrations of [vitamin E tocotrienols].” Cell studies such as this are the first step in a clinical investigation and need to be confirmed in first animal and then human studies.
Source: Khanna et al. Nanomolar vitamin E alpha-tocotrienol inhibits glutamate-induced activation of phospholipase A2 and causes neuroprotection. J Neurochem. 2010 Mar;112(5):1240-1260
© 2010 The Authors
Posted February 24, 2010.
References:
- Khanna S., Patel V., Rink C., Roy S. and Sen C. K. (2005a) Delivery of orally supplemented alpha-tocotrienol to vital organs of rats and tocopherol-transport protein deficient mice. Free Radic Biol Med 39, 1310-1319.
- Khanna S., Roy S., Parinandi N. L., Maurer M. and Sen C. K. (2006) Characterization of the potent neuroprotective properties of the natural vitamin E alpha-tocotrienol. J Neurochem 98, 1474-1486.
- Khanna S., Roy S., Ryu H., Bahadduri P., Swaan P. W., Ratan R. R. and Sen C. K. (2003) Molecular basis of vitamin E action: tocotrienol modulates 12-lipoxygenase, a key mediator of glutamate-induced neurodegeneration. J Biol Chem 278, 43508-43515.
- “About Stroke” posted on the National Institutes of Health Website.
- Khanna S. Nanomolar vitamin E -tocotrienol inhibits glutamate-induced activation of phospholipase A2 and causes neuroprotection. Jou Neurochemistry 2009. Accepted Article Online: Dec 17 2009.
- Sun G. Y., Xu J., Jensen M. D. and Simonyi A. (2004) Phospholipase A2 in the central nervous system: implications for neurodegenerative diseases. J Lipid Res 45, 205-213.
