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Vitamin E/Coenzyme Q-Dependent "Free Radical Reductases": Redox Regulators in Ferroptosis.
Kagan, Valerian E; Straub, Adam C; Tyurina, Yulia Y; Kapralov, Alexandr A; Hall, Robert; Wenzel, Sally E; Mallampalli, Rama K; Bayir, Hülya.
Affiliation
  • Kagan VE; Center for Free Radical and Antioxidant Health, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
  • Straub AC; Department of Environmental Health and Pharmacology and Chemical Biology and University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
  • Tyurina YY; Department of Radiation Oncology and Chemistry, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
  • Kapralov AA; Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
  • Hall R; Heart, Lung, Blood, and Vascular Medicine Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
  • Wenzel SE; Center for Free Radical and Antioxidant Health, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
  • Mallampalli RK; Department of Environmental Health and Pharmacology and Chemical Biology and University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
  • Bayir H; Center for Free Radical and Antioxidant Health, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Antioxid Redox Signal ; 40(4-6): 317-328, 2024 02.
Article in En | MEDLINE | ID: mdl-37154783
ABSTRACT

Significance:

Lipid peroxidation and its products, oxygenated polyunsaturated lipids, act as essential signals coordinating metabolism and physiology and can be deleterious to membranes when they accumulate in excessive amounts. Recent Advances There is an emerging understanding that regulation of polyunsaturated fatty acid (PUFA) phospholipid peroxidation, particularly of PUFA-phosphatidylethanolamine, is important in a newly discovered type of regulated cell death, ferroptosis. Among the most recently described regulatory mechanisms is the ferroptosis suppressor protein, which controls the peroxidation process due to its ability to reduce coenzyme Q (CoQ). Critical Issues In this study, we reviewed the most recent data in the context of the concept of free radical reductases formulated in the 1980-1990s and focused on enzymatic mechanisms of CoQ reduction in different membranes (e.g., mitochondrial, endoplasmic reticulum, and plasma membrane electron transporters) as well as TCA cycle components and cytosolic reductases capable of recycling the high antioxidant efficiency of the CoQ/vitamin E system. Future Directions We highlight the importance of individual components of the free radical reductase network in regulating the ferroptotic program and defining the sensitivity/tolerance of cells to ferroptotic death. Complete deciphering of the interactive complexity of this system may be important for designing effective antiferroptotic modalities. Antioxid. Redox Signal. 40, 317-328.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Ubiquinone / Ferroptosis Language: En Journal: Antioxid Redox Signal Journal subject: METABOLISMO Year: 2024 Type: Article Affiliation country: United States

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Ubiquinone / Ferroptosis Language: En Journal: Antioxid Redox Signal Journal subject: METABOLISMO Year: 2024 Type: Article Affiliation country: United States