Vitamin E Supports Brain Health After Stroke
Lee Swanson Research Update
Alpha-tocotrienol, one of eight forms of vitamin E, was found to inhibit an enzyme from releasing fatty acids that eventually kill neurons, according to findings from a study with mouse brain cells published in the Journal of Neurochemistry.
"Our research suggests that the different forms of natural vitamin E have distinct functions. The relatively poorly-studied tocotrienol form of natural vitamin E targets specific pathways to protect against neural cell death and rescues the brain after stroke injury," said Prof. Chandan Sen, lead researcher of the study. "Here, we identify a novel target for tocotrienol that explains how neural cells are protected."
"We have studied an enzyme that is present all the time, but one that is activated after a stroke in a way that causes neurodegeneration. We found that it can be put in check by very low levels of tocotrienol," he said. "So what we have here is a naturally-derived nutrient that provides this beneficial impact."
Sen and his co-workers looked at the effects of alpha-tocotrienol in inhibiting the action of the enzyme called cytosolic calcium-dependent phospholipase A2, or cPLA2. Following the trauma of blocked blood flow associated with a stroke, an excessive amount of the neurotransmitter glutamate is released in the brain. Despite playing an important role in learning and memory, too much glutamate can trigger the death of brain cells, or neurons, said to be the most damaging effects of a stroke.
By introducing excess glutamate into the brain cells of mice, the Ohio-based researchers mimicked the brain’s environment after a stroke. In the presence of excess glutamate, cPLA2 released arachidonic acid into the brain, which subsequently underwent an enzymatic chemical reaction to become toxic.
When tocotrienol was introduced to cells exposed to the high levels of glutamate, arachidonic acid levels decreased by 60%, said the researchers. This resulted in a cell survival rate four times higher than cells exposed to glutamate alone.
Prof. Sen noted that the effects were observable with a 250 nanomolar dose of tocotrienol. This is equivalent to a concentration about 10 times lower than the average amount of tocotrienol circulating in humans who consume the vitamin regularly.
"On a concentration basis, this finding represents the most potent of all biological functions exhibited by any natural vitamin E molecule," wrote the researchers in the Journal of Neurochemistry. "This work provides first evidence in recognizing inducible cPLA2 activity as a key target of tocotrienol in protecting against glutamate-induced neurotoxicity," they added.
Journal of Neurochemistry Published online ahead of print.
Jan. 2010
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