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Specifically, selenomethionine confers ferroptosis protection through two distinct pathways : (1) a GPX4-dependent mechanism involving selenium provision via multiple metabolic routes to sustain GPX4 biosynthesis, and (2) a GPX4-independent mechanism mediated through direct ROS scavenging via its intrinsic redox-active properties

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There is no benefit to exceeding your requirement, and with selenium, the gap between "enough" and "too much" is unusually small

Targeting PCSK9 to upregulate MHC-II on the surface of tumor cells in tumor immunotherapy