Yeast as a model system to study metabolic impact of selenium compounds
Authors:Enrique Herrero1,* and Ralf Erik Wellinger2
1 Departament de Ciències Mèdiques Bàsiques, Universitat de Lleida, IRBLleida, Rovira Roure 80, 25198 Lleida, Spain.
2 Centro Andaluz de Biología Molecular y Medicina Regenerativa (CABIMER), Universidad de Sevilla, 41092 Sevilla, Spain.
Keywords:
selenium, yeast, DNA damage, oxidative stress, mitochondrial function, signal transduction
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Conflict of interest statement:
The authors declare no conflict of interest.
Please cite this article as:
Enrique Herrero and Ralf Erik Wellinger (2015). Yeast as a model system to study metabolic impact of selenium compounds. Microbial Cell 2(5): 139-149.
© 2015 Herrero and Wellinger. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.
Abstract:
Inorganic Se forms such as selenate or selenite (the two more abundant forms in nature) can be toxic in Saccharomyces cerevisiae cells, which constitute an adequate model to study such toxicity at the molecular level and the functions participating in protection against Se compounds. Those Se forms enter the yeast cell through other oxyanion transporters. Once inside the cell, inorganic Se forms may be converted into selenide through a reductive pathway that in physiological conditions involves reduced glutathione with its consequent oxidation into diglutathione and alteration of the cellular redox buffering capacity. Selenide can subsequently be converted by molecular oxygen into elemental Se, with production of superoxide anions and other reactive oxygen species. Overall, these events result in DNA damage and dose-dependent reversible or irreversible protein oxidation, although additional oxidation of other cellular macromolecules cannot be discarded. Stress-adaptation pathways are essential for efficient Se detoxification, while activation of DNA damage checkpoint and repair pathways protects against Se-mediated genotoxicity. We propose that yeast may be used to improve our knowledge on the impact of Se on metal homeostasis, the identification of Se-targets at the DNA and protein levels, and to gain more insights into the mechanism of Se-mediated apoptosis.
doi: 10.15698/mic2015.05.200
Volume 2, pp. 139 to 149, published 08/04/2015.