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Selenium: Tracing another essential element of ferroptotic cell death.

Cell Chem. Bio. 27, 409-419 (2020)
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The trace elements iron and selenium play decisive roles in a distinct form of necrotic cell death, known as ferroptosis. While iron promotes ferroptosis by contributing to Fenton-type reactions and uncontrolled lipid autoxidation, the hallmark of ferroptosis, selenium in the form of glutathione peroxidase 4 (GPX4), subdues phospholipid peroxidation and associated cell death. Beyond the canonical cystine/glutamate antiporter system x(c)(-)/glutathione/GPX4 nexus, recent studies unveiled the second mainstay in ferroptosis entailing extra-mitechondriai ubiquinone, ferroptosis suppressor protein 1, and NAD(P)H as electron donor. Unlike GPX4, this selenium- and thiol-independent system acts on the level of peroxyl radicals in membranes thereby restraining Hold peroxidation. Therefore, ferroptosis is a multifaceted cell-death paradigm characterized by several metabolic networks, whereby metabolic dyshomeostasis may cause ferroplotic cell death and organ failure. Here, we discuss the basic features of ferroptosis with a focus on selenium, offering exciting opportunities to control diseases linked to ferroptosis, including transient ischemia reperfusion and neurodegeneration.
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Publication type Article: Journal article
Document type Review
Keywords Ferroptosis ; Ferroptosis Suppressor Protein 1 ; Glutathione Peroxidase 4 ; Pufa ; Selenium; Glutathione-peroxidase 4; Active Organoselenium Compound; Selenoprotein-p; Vitamin-e; Lipid-peroxidation; Cancer Prevention; Thioredoxin Reductase; Selenocysteine Insertion; Targeted Disruption; Prostate-cancer
ISSN (print) / ISBN 2451-9448
e-ISSN 2451-9456
Quellenangaben Volume: 27, Issue: 4, Pages: 409-419 Article Number: , Supplement: ,
Publisher Cell Press
Publishing Place Cambridge, Massachusetts
Reviewing status Peer reviewed