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Vitamin E Tocotrienol Complex Protects Against Stroke-Induced Neurodegeneration

The publication of the NIH-funded study conducted at the Ohio State University Medical Center that confirms earlier studies suggests that natural full spectrum palm tocotrienol complex may significantly benefit stroke-induced neurodegeneration.

Published in the October 2005 issue of the American Heart Association’s journal STROKE, Vitamin E tocotrienols showed significant protection against stroke-induced injury compared with matched controls.

In a previous study, Professor Chandan Sen from the Ohio State University Medical Center showed that tocotrienol crosses the blood-brain barrier and in neuronal cells, nanomolar level of alpha-tocotrienol but not alpha-tocopherol blocked glutamate-induced cell death. Glutamate-induced toxicity is a major contributor to pathological cell death within the nervous system.

In the current study, to further explore the effects of tocotrienol and its neuroprotective mechanism, the researchers supplemented spontaneously-hypertensive rats with Tocomin® brand natural palm tocotrienol complex. The animal model chosen for the trial is commonly used in stroke research as hypertension represents one of the major risk factors for stroke. The brain infarct volume was measured 24 hours subsequent to stroke.

Oral supplementation with tocotrienols in spontaneously-hypertensive rats led to increased brain levels of tocotrienols. This unique form of vitamin E at subattomole quantity protected neurons from glutamate-challenge, consistent with previous reports that at low doses, the neuroprotective property of tocotrienol is not shared by tocopherol. Alpha-tocopherol itself had no effect at such low doses.

Rats supplemented with tocotrienols showed more protection against stroke-induced injury compared to unsupplemented controls. The neuroprotective effect was associated with suppression of stroke-associated c-Src activation, which is a key mechanism that contributes to neurodegeneration. Next, Prof. Sen went on to identify that 12-lipoygenase as another tocotrienol-sensitive molecular check-point that proved to be critical in executing neuron deaths. Tocotrienol lowers the tyrosine phosphorylation of 12-lipoxygenase and hence protects the neurons from apoptosis. The site of action is in the cytosol and not nuclear.

This study demonstrates that oral supplementation with tocotrienols may protect against stroke. Tocotrienols effectively modulates two key molecular check-points - the c-Src and 12-lipoxygenase activity to favor survival of the neurons

“Eighty three years after the discovery of vitamin E in 1922, it is long overdue to closely examine all naturally occurring forms of vitamin E side by side,” said Prof. Sen, who noted that the general misconception is that tocopherols are the only vitamin E molecules in nature. “Attention to the naturally occurring tocotrienols, especially to their neuroprotective properties, could well provide us with a powerful tool to combat neurodegeneration especially stroke, by safe dietary means”.

Maximum Vitality contains all the tocopherol and tocotrienol forms of Vitamin E.


BACKGROUND AND PURPOSE: The current work is based on our previous finding that in neuronal cells, nmol/L concentrations of alpha-tocotrienol (TCT), but not alpha-tocopherol (TCP), blocked glutamate-induced death by suppressing early activation of c-Src kinase and 12-lipoxygenase. METHODS: The single neuron microinjection technique was used to compare the neuroprotective effects of TCT with that of the more widely known TCP. Stroke-dependent brain tissue damage was studied in 12-Lox-deficient mice and spontaneously hypertensive rats orally supplemented with TCT. RESULTS: Subattomole quantity of TCT, but not TCP, protected neurons from glutamate challenge. Pharmacological as well as genetic approaches revealed that 12-Lox is rapidly tyrosine phosphorylated in the glutamate-challenged neuron and that this phosphorylation is catalyzed by c-Src. 12-Lox-deficient mice were more resistant to stroke-induced brain injury than their wild-type controls. Oral supplementation of TCT to spontaneously hypertensive rats led to increased TCT levels in the brain. TCT-supplemented rats showed more protection against stroke-induced injury compared with matched controls. Such protection was associated with lower c-Src activation and 12-Lox phosphorylation at the stroke site. CONCLUSIONS: The natural vitamin E, TCT, acts on key molecular checkpoints to protect against glutamate- and stroke-induced neurodegeneration.


Khanna S, Roy S, Slivka A, Craft TK, Chaki S, Rink C, Notestine MA, DeVries AC, Parinandi NL, Sen CK. Neuroprotective properties of the natural vitamin E alpha-tocotrienol. Stroke. 2005 Oct;36(10):2258-64. Epub 2005 Sep 15. PMID: 16166580 [PubMed - indexed for MEDLINE]

Key concepts: Vitamin E, tocotrienols, stroke