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Reference: Izquierdo A, et al. (2010) Selenite-induced cell death in Saccharomyces cerevisiae: protective role of glutaredoxins. Microbiology 156(Pt 9):2608-20

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Abstract

In contrast to higher organisms, selenium is not essential for growth in Saccharomyces cerevisiae. In this species, it causes toxic effects at high concentrations. In the present study, we show that when supplied as selenite to yeast cultures, its effects can be dissected into two death phases. From initial treatment times, it causes loss of membrane integrity and genotoxicity. Both effects occur at higher levels in mutants lacking Grx1 and Grx2 than in wild type cells, and are reversed by expression of a cytosolic version of the membrane-associated Grx7 glutaredoxin. Grx7 can also rescue the high levels of protein carbonylation damage occurring in selenite-treated cultures of the grx1 grx2 mutant. At advances times, selenite causes abnormal nuclear morphology and appearance of TUNEL-positive cells, which are considered apoptotic markers in yeast cells. This effect is independent of Grx1 and Grx2. Therefore, the protective role of both glutaredoxins is circumscribed to the initial stages of selenite treatment. Lack of Yca1 metacaspase or of a functional mitochondrial electron transport chain only moderately diminishes apoptotic-like death by selenite. In contrast, selenite-induced apoptosis is dependent on the apoptosis-inducing factor Aif1. In the absence of the latter, intracellular protein carbonylation is reduced after prolonged selenite treatment, supporting that part of the oxidative damage is contributed by apoptotic cells.

Reference Type
Journal Article
Authors
Izquierdo A, Casas C, Herrero E
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