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Review

Programmed Cell-Death by Ferroptosis: Antioxidants as Mitigators

1
Nutrition and Obesity Group, Department of Nutrition and Food Sciences, University of the Basque Country (UPV/EHU), 01006 Vitoria, Spain
2
King’s College London, Department of Nutritional Sciences, Faculty of Life Sciences and Medicine, Franklin-Wilkins Building, 150 Stamford Street, London SE1 9NH, UK
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2019, 20(19), 4968; https://doi.org/10.3390/ijms20194968
Received: 9 September 2019 / Revised: 29 September 2019 / Accepted: 2 October 2019 / Published: 8 October 2019
(This article belongs to the Section Bioactives and Nutraceuticals)
Iron, the fourth most abundant element in the Earth’s crust, is vital in living organisms because of its diverse ligand-binding and electron-transfer properties. This ability of iron in the redox cycle as a ferrous ion enables it to react with H2O2, in the Fenton reaction, to produce a hydroxyl radical (•OH)—one of the reactive oxygen species (ROS) that cause deleterious oxidative damage to DNA, proteins, and membrane lipids. Ferroptosis is a non-apoptotic regulated cell death that is dependent on iron and reactive oxygen species (ROS) and is characterized by lipid peroxidation. It is triggered when the endogenous antioxidant status of the cell is compromised, leading to lipid ROS accumulation that is toxic and damaging to the membrane structure. Consequently, oxidative stress and the antioxidant levels of the cells are important modulators of lipid peroxidation that induce this novel form of cell death. Remedies capable of averting iron-dependent lipid peroxidation, therefore, are lipophilic antioxidants, including vitamin E, ferrostatin-1 (Fer-1), liproxstatin-1 (Lip-1) and possibly potent bioactive polyphenols. Moreover, most of the enzymes and proteins that cascade or interact in the pathway of ferroptosis such as a subunit of the cystine/glutamate transporter xc (SLC7A11), glutathione peroxidase 4 (GPX4), and the glutamate–cysteine ligase (GCLC) iron metabolism genes transferrin receptor 1 (TfR1) ferroportin, (Fpn) heme oxygenase 1 (HO-1) and ferritin are regulated by the antioxidant response element of the transcription factor, Nrf2. These, as well as other radical trapping antioxidants (RTAs), are discussed in the current review. View Full-Text
Keywords: ferroptosis; antioxidants; glutathione; iron ferroptosis; antioxidants; glutathione; iron
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MDPI and ACS Style

Kajarabille, N.; Latunde-Dada, G.O. Programmed Cell-Death by Ferroptosis: Antioxidants as Mitigators. Int. J. Mol. Sci. 2019, 20, 4968. https://doi.org/10.3390/ijms20194968

AMA Style

Kajarabille N, Latunde-Dada GO. Programmed Cell-Death by Ferroptosis: Antioxidants as Mitigators. International Journal of Molecular Sciences. 2019; 20(19):4968. https://doi.org/10.3390/ijms20194968

Chicago/Turabian Style

Kajarabille, Naroa, and Gladys O. Latunde-Dada 2019. "Programmed Cell-Death by Ferroptosis: Antioxidants as Mitigators" International Journal of Molecular Sciences 20, no. 19: 4968. https://doi.org/10.3390/ijms20194968

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