In mice, the brain exhibits a distinct selenoprotein expression profile characterized by delayed and attenuated postnatal upregulation of antioxidant genes relative to other organs, indicating specialized mechanisms for maintaining selenium homeostasis and protecting against oxidative stress in this metabolically active but vulnerable tissue.

After birth, the brain slowly increases its production of selenium-based protective proteins because it needs to conserve selenium for critical survival functions first, while other organs quickly use selenium to fight new oxidative stress. The liver sends selenium to the brain through a transport protein, and the brain uses it to maintain essential proteins that prevent cell damage, especially in energy-producing areas, even when overall selenium levels are low.