With that extra glutamate present, the cPLA2 enzyme releases a fatty acid called arachidonic acid into the brain. Under normal conditions, this fatty acid is housed within lipids that help maintain cell membrane stability.

But when it is free-roaming, arachidonic acid undergoes an enzymatic chemical reaction that makes it toxic - the final step before brain cells are poisoned in this environment and start to die. Activation of the cPLA2 enzyme is required to release the damaging fatty acid in response to insult caused by high levels of glutamate.

Sen and colleagues introduced the tocotrienol vitamin E to the cells that had already been exposed to excess glutamate. The presence of the vitamin decreased the release of fatty acids by 60 percent when compared to cells exposed to glutamate alone.

Brain cells exposed to excess glutamate followed by tocotrienol fared much better, too, compared to those exposed to only the damaging levels of glutamate. Cells treated with TCT were almost four times more likely to survive than were cells exposed to glutamate alone.

Though cPLA2 exists naturally in the body, blocking excessive function of this enzyme is not harmful, Sen explained. Scientists have already determined that mice genetically altered so they cannot activate the enzyme achieve their normal life expectancy and carry a lower risk for stroke.

Sen also noted that the amount of tocotrienol needed to achieve these effects is quite small - just 250 nanomolar, a concentration about 10 times lower than the average amount of tocotrienol circulating in humans who consume the vitamin regularly.

"So you don't have to gobble up a lot of the nutrient to see these effects," he said.

Source: Ohio State University