COLUMBUS, Ohio—Blocking the function of an enzyme in the brain with the tocotrienol (TCT) form of vitamin E can prevent nerve cells from dying after a stroke, according to a new study from Ohio State University.
Researchers discovered tocotrienol vitamin E’s ability to protect the brain 10 years ago; however, this current study offers the most specific details about how that protection works. They had linked TCT’s effects to various substances that are activated in the brain after a stroke before they concluded that the enzyme cystolic calcium-dependent phospholipase A2, or cPLA2 could serve as an important therapeutic target.
Following the trauma of blocked blood flow associated with a stroke, an excessive amount of glutamate is released in the brain. Glutamate is a neurotransmitter that, in tiny amounts, has important roles in learning and memory. Too much of it triggers a sequence of reactions that lead to the death of brain cells.
Researchers introduced excess glutamate to the cells to mimic the brain’s environment after a stroke. 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. Activation of the cPLA2 enzyme is required to release the damaging fatty acid in response to insult caused by high levels of glutamate.
Researchers introduced the tocotrienol vitamin E to the cells that already had 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 TCT 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.
Researches also noted that the amount of TCT needed to achieve these effects is quite small—just 250 nanomolar, a concentration about 10 times lower than the average amount of TCT circulating in humans who consume the vitamin regularly.
