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Uncovering the Cellular Protection Mechanism of Selenium: Professor Do-Hoon Kim’s Breakthrough Research

Professor Do-Hoon Kim’s research group at the University of Massachusetts Medical School has discovered the cellular protection mechanism of selenium, known for its antioxidant properties.

Professor Do-Hoon Kim, University of Massachusetts Medical School

Until now, selenium was only known as an antioxidant mechanism as a component of “selenoprotein”, but the metabolism discovered by researchers this time is that selenium, known only as an intermediate product in the synthesis process of selenoprotein, directly causes oxidation and reduction of reactions inside and outside the cell. It’s a mechanism.

The research team hypothesized that toxic metabolites would be created during cellular metabolism and then immediately disappear, and proposed a strategy to treat diseases using them.

Professor Do-Hoon Kim published a study on selenide, a toxic metabolite that appears in the selenium metabolism pathway, in Nature Metabolism in 2020. This study showed that when selenide is present at a concentration below the toxic one, it occurs cell death. function that protects cells by preventing

Selenium is a powerful antioxidant. It combines with the amino acid cysteine ​​to create selenocysteine, a component of selenoprotein, and functions as an antioxidant, including glutathione peroxidase.

In particular, selenoprotein inhibits ferroptosis, a cell death mechanism, by preventing the production of lipid peroxides. Ferroptosis is an iron-dependent cell death mechanism caused by oxygen radicals peroxidizing cell membranes.

Unlike the selenoprotein metabolism known so far, the new metabolism discovered by the research team begins with “selenide”, a hydrogen bond with selenium, which provides electrons to coenzyme Q10, a coenzyme involved in oxidation and reduction. Reduced coenzyme Q10 protects cells from ferroptosis by preventing the peroxidation of the lipids that make up the cell membrane.

The research team also revealed that the reductive metabolism of selenide coenzyme Q10 occurs by an enzyme called SQOR (sulfide quinone oxidorductase).

Professor Kim Do-hoon said: “The “toxicity” of toxic metabolites is seen as a phenomenon in which normal mechanisms are overactivated. “Selenide is an important basis for this concept, and in the future we may be able to find unknown normal functions in other toxic metabolites,” he said. “Ferroptosis plays an important role in the survival of tumor cells and is also related to various other diseases.” . “By activating the mechanism discovered in this study, we will be able to protect cells in situations such as ischemic damage or, conversely, we will be able to eliminate tumor cells by suppressing the mechanism,” he predicted.

The results of this study, conducted with the support of the Seo Kyung-bae Science Foundation, were published in the international academic journal “Nature Metabolism”.

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