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Biol. Chem., Vol. 388, pp. 1007–1017, October 2007 • Copyright by Walter de Gruyter • Berlin • New York. DOI 10.1515/BC.2007.126 2007/196 Article in press - uncorrected proof Review Molecular biology of glutathione peroxidase 4: from genomic structure to developmental expression and neural function Nicolai E. Savaskan1,2,*, Christoph Ufer3, Hartmut Kühn3 and Astrid Borchert3 1 Division of Cellular Biochemistry, The Netherlands Cancer Institute, NL-1066 CX Amsterdam, The Netherlands 2 Brain Research Institute, Department of Neuromorphology, ETH and University of

embryogen- esis, and a contribution to sperm chromatin condensa- tion. The expression of three forms of PHGPx and early embryonic lethality call for more specific studies, such as tissue-specific disruption of PHGPx, to precisely under- stand the contribution of PHGPx to mammalian physio- logy and under pathological conditions. Keywords: glutathione peroxidase 4; lipid peroxidation; selenoprotein; spermatogenesis; thiol peroxidase. Introduction A quarter of a century ago, Ursini et al. (1982) purified a protein from pig liver displaying peroxidative activity towards

Abstract

Ferroptosis is a recently identified form of regulated cell death that differs from other known forms of cell death morphologically, biochemically, and genetically. The main properties of ferroptosis are free redox-active iron and consequent iron-dependent peroxidation of polyunsaturated fatty acids in cell membrane phospholipids, which results in the accumulation of lipid-based reactive oxygen species due to loss of glutathione peroxidase 4 activity. Ferroptosis has increasingly been associated with neurodegenerative diseases, carcinogenesis, stroke, intracerebral haemorrhage, traumatic brain injury, and ischemia-reperfusion injury. It has also shown a significant therapeutic potential in the treatment of cancer and other diseases. This review summarises current knowledge about and the mechanisms that regulate ferroptosis.

; glutathione peroxidase 4; selenoprotein 15; selenoprotein P; thyroglobulin. Present address: Max-Planck-Institut für Molekulare Genetik,a Fabeckstr. 60-62, D-14195 Berlin, Germany. Introduction: the thyroid gland, thyroid hormones and selenium The main physiological function of the thyroid gland is the synthesis of thyroid hormones (TH), for which it is the exclusive source in the vertebrate body. THs are key regulators of development, growth, and differentiation, particularly of the nervous system, as well as many phys- iological processes in the adult, such as body

superoxide-dismutase and in the concentration of copper in the blood in various breed crosses of sheep. Res. Vet. Sci., 34, 253-256. Wunderink, R., Waterer, G. (2014). Clinical practice. Community-acquired pneumonia. New Engl. J. Med., 370 (6), 543-551. Yoo, M., Gu, X., Xu, X., Kim, J., Carlson, B., Patterson, A., Cai, H., Gladyshev, V., Hatfield, D. (2010). Delineating the role of glutathione peroxidase 4 in protecting cells against lipid hydroperoxide damage and in Alzheimer’s disease. Antioxid. Redox. Signal., 12, 819-827.

membrane lipid repair, leading to the accumulation of reactive oxygen species (ROS) on membrane lipids [ 31 , 32 , 33 ] and eventually leading to cell death. Ferroptosis requires the simultaneous depletion of glutathione (GSH) or inactivation of GSH-dependent antioxidant enzyme glutathione peroxidase 4 (GPX4) and the incorporation of oxidizable polyunsaturated fatty acids into phospholipids [ 34 ], and the process of iron-dependent cell death is accompanied by inflammatory manifestations. Therefore, the aim of this study was to investigate the antioxidant effects of EGCG

melatonin on PCB (Aroclor 1254) induced neuronal damage and changes in Cu/Zn superoxide dismutase and glutathione peroxidase-4 mRNA expression in cerebral cortex, cerebellum and hippocampus of adult rats. Neurosci Res 2010;66:189–97. doi: 10.1016/j.neures.2009.10.015

neuronal damage and changes in Cu/Zn superoxide dismutase and glutathione peroxidase-4 mRNA expression in cerebral cortex, cerebellum and hippocampus of adult rats. Neurosci Res 66 : 189-197. Venkataraman P, Krishnamoorthy G, Vengatesh G, Srinivasan N, Aruldhas MM, Arunakaran J. (2008). Protective role of melatonin on PCB (Aroclor 1,254) induced oxidative stress and changes in acetylcholine esterase and membrane bound ATPases in cerebellum, cerebral cortex and hippocampus of adult rat brain. Int J Dev Neurosci 26 : 585-591. Wang X. (2001). The expanding role of

on the expression profi le of SRA1, a novel member of pre-mRNA splicing factors, in HL-60 human promyelocytic leukemia cells 388, 773–778 Reisenauer, A., O. Eickelberg, A. Wille, A. Heimburg, A. Reinhold, B.F. Sloane, T. Welte and F. Bühling Increased carcinogenic potential of myeloid tumor cells induced by aberrant TGF-β1-signaling and upregulation of cathepsin B 388, 639–650 Savaskan, N.E., C. Ufer, H. Kühn and A. Borchert Molecular biology of glutathione peroxidase 4: from genomic structure to developmental expression and neural function 388, 1007

, S., Kaifu, T., Takai, T., and Obinata, M. (2007). Increased susceptibility of MER5 (peroxiredoxin III) knockout mice to LPS-induced oxidative stress. Biochem. Biophys. Res. Commun. 355 , 715–721. Li, L., Kaifu, T., Obinata, M., and Takai, T. (2009). Peroxiredoxin III-deficiency sensitizes macrophages to oxidative stress. J. Biochem. 145 , 425–427. Liang, H., Yoo, S.E., Na, R., Walter, C.A., Richardson, A., and Ran, Q. (2009). Short form glutathione peroxidase 4 is the essential isoform required for survival and somatic mitochondrial functions. J. Biol. Chem