Peer-Reviewed Publication
Nat Metab2024;6(2):343-358.February 1, 2024Journal Article
Selenium reduction of ubiquinone via SQOR suppresses ferroptosis.
Namgyu Lee1,2, Sung Jin Park3, Mike Lange4,5, Tenzin Tseyang3, Mihir B Doshi6, Tae Yong Kim7, Yoseb Song8, Dong In Kim7, Paul L Greer3, James A Olzmann4,5,9, Jessica B Spinelli3, Dohoon Kim10
1Department of Molecular, Cell and Cancer Biology, University of Massachusetts Chan Medical School, Worcester, MA, USA. namgyu.lee@dankook.ac.kr.
2Department of Biomedical Science & Engineering, Dankook University, Cheonan, Republic of Korea. namgyu.lee@dankook.ac.kr.
3Program in Molecular Medicine, University of Massachusetts Chan Medical School, Worcester, MA, USA.
4Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA, USA.
5Department of Nutritional Sciences and Toxicology, University of California, Berkeley, Berkeley, CA, USA.
6Department of Biomedical Science & Engineering, Dankook University, Cheonan, Republic of Korea.
7Standigm, Inc., Seoul, Republic of Korea.
8Department of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
9Chan Zuckerberg Biohub, San Francisco, CA, USA.
10Department of Molecular, Cell and Cancer Biology, University of Massachusetts Chan Medical School, Worcester, MA, USA. dohoon.kim@umassmed.edu.
Abstract
The canonical biological function of selenium is in the production of selenocysteine residues of selenoproteins, and this forms the basis for its role as an essential antioxidant and cytoprotective micronutrient. Here we demonstrate that, via its metabolic intermediate hydrogen selenide, selenium reduces ubiquinone in the mitochondria through catalysis by sulfide quinone oxidoreductase. Through th…
Create a free account to keep reading
Free members get 10 full research views every month across publications, clinical trials, FDA clearances, adverse events, and NIH grants. No credit card required.
Want unlimited research access? See Pro plans