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Redox biology

Selenium abandons selenoproteins to inhibit ferroptosis rapidly

Nature Metabolism volume 6, pages 200–202 (2024)Cite this article

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Selenium is usually incorporated into selenoproteins, with important functions in redox regulation. A new study in Nature Metabolism reveals a previously unappreciated role for selenium-based chemical species as direct electron donors to reduce ubiquinone, thus contributing to redox homeostasis by preventing lipid peroxidation.

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Fig. 1: Pharmacological selenium targets the effector phase of ferroptosis (lipid peroxidation) via sulfide quinone oxidoreductase (SQOR) or GPX4.

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Authors and Affiliations

  1. Burke Neurological Institute, Weill Cornell Medicine, White Plains, NY, USA

    Ian G. Chambers & Rajiv R. Ratan

  2. Department of Neurology and the Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, USA

    Rajiv R. Ratan

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  1. Ian G. Chambers
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  2. Rajiv R. Ratan
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Correspondence to Rajiv R. Ratan.

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Competing interests

R.R.R. is an inventor on a composition of matter and a method of use patent related to the use of selenium-containing peptides for treatment of stroke granted by the United States Patent and Trademark Office (Application # 17363140). He is collaborating with Celdara Medical Inc. to advance this technology for the treatment of hemorrhagic stroke. I.G.C. declares no competing interests.

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Chambers, I.G., Ratan, R.R. Selenium abandons selenoproteins to inhibit ferroptosis rapidly. Nat Metab 6, 200–202 (2024). https://doi.org/10.1038/s42255-024-00980-6

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