Selenomethionine decreases markers of oxidative damage and cell death in human cancer cells under conditions that trigger ferroptosis, such as exposure to RSL3 or lack of cystine.

Selenomethionine, a form of selenium, can still prevent cell damage and death in human cells even when the GPX4 protein is completely removed, suggesting it blocks a type of cell death called ferroptosis through a different pathway than previously thought.

Selenomethionine can neutralize reactive oxygen species by undergoing a chemical reaction that produces selenomethionine sulfoxide, and this process reduces ferroptosis without requiring the synthesis of new proteins.

Selenomethionine raises the levels of the GPX4 protein in specific human cells grown in the lab when those cells are stressed by lack of cystine or exposure to RSL3, and this effect occurs even when two key enzymes in the transsulfuration pathway are blocked.