Selenium protects a specific type of interneurons from epileptic seizures

Selenium protects a specific type of interneurons from epileptic seizures

Scientists have been investigating for years the processes of a novel type of cell death, known as ferroptosis. In this context, the enzyme GPX4, which normally contains selenium in the form of the amino acid selenocysteine, plays an important role.

In order to better understand the role of GPX4 in this death process, authors studied mouse models in which the enzyme was modified," said study leader. "In one of these models, we observed that mice with a replacement of selenium to sulfur in GPX4 did not survive for longer than three weeks due to neurological complications."

In their search for the underlying reasons, the researchers identified a distinct subpopulation of specialized neurons in the brain, which were absent when selenium-containing GPX4 was lacking. "In further studies, we were able to show that these neurons were lost during postnatal development, when sulfur- instead of selenium-containing GPX4 was present," stated first author of the study.

Furthermore, the scientists were able to show that ferroptosis is triggered by oxidative stress, which is known to occur for instance during high metabolic activity of cells and high neuronal activity. "Our study demonstrates for the first time that selenium is an essential factor for the postnatal development of a specific type of interneurons," said the author. "Selenium-containing GPX4 protects these specialized neurons from oxidative stress and from ferroptotic cell death."

Thus, the study explains why certain selenoenzymes are essential in some organisms, including mammals, whereas they are dispensable in other organisms, such as fungi and higher plants. In future investigations, study leader aim to investigate how ferroptosis is triggered in cells.