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. 2020 Nov 23;124(5):862–879. doi: 10.1038/s41416-020-01156-1

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — a Drugs targeting cysteine metabolism. b Key inhibition targets and interplay between the trans-sulphuration pathway, the xCT antiporter and ferroptosis. c Inhibition of glutathione- and thioredoxin-dependent antioxidant pathways by sulphasalazine or auranofin combined with L-BSO. d Novel selenium-chrysin nanoformulations acting as inhibitors of glutathione bioavailability/synthesis and CBS activity. CBS cystathionine β-synthase, CSE cystathionine γ-lyase, GCS γ-glutamyl cysteine synthetase, GSS glutathione synthetase, Pyr pyruvate, α-KB α-ketobutyrate, GSH glutathione reduced form, GSSG glutathione oxidised form, ROS reactive oxygen species, FIN ferroptosis-inducing compounds.