Reactive oxygen species and yeast apoptosis

Perrone, Gabriel G.; Tan, Shi‐Xiong; Dawes, Ian W.

doi:10.1016/j.bbamcr.2008.01.023

Cited by 353 publications

(275 citation statements)

References 172 publications

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“…An excess of ROS can cause damage to numerous cellular components, including nucleic acids and lipids. In recent years, it has become evident that ROS also play an important signaling role controlling and regulating some biological processes, such as growth, development, response to biotic and abiotic environmental stimuli and programmed cell death (Perrone et al 2008;Scott and Eaton 2008). To control ROS toxicity and to enable ROS to act as signaling molecules, cells have developed a variety of antioxidant systems to efficiently scavenge ROS excess and to keep ROS production and scavenging systems in balance.…”

Section: Introductionmentioning

confidence: 99%

Characterization of a CuZn superoxide dismutase gene in the arbuscular mycorrhizal fungus Glomus intraradices

et al. 2010

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To gain further insights into the mechanisms of redox homeostasis in arbuscular mycorrhizal fungi, we characterized a Glomus intraradices gene (GintSOD1) showing high similarity to previously described genes encoding CuZn superoxide dismutases (SODs). The GintSOD1 gene consists of an open reading frame of 471 bp, predicted to encode a protein of 157 amino acids with an estimated molecular mass of 16.3 kDa. Functional complementation assays in a CuZnSOD-defective yeast mutant showed that GintSOD1 protects the yeast cells from oxygen toxicity and that it, therefore, encodes a protein that scavenges reactive oxygen species (ROS). GintSOD1 transcripts differentially accumulate during the fungal life cycle, reaching the highest expression levels in the intraradical mycelium. GintSOD1 expression is induced by the well known ROS-inducing agents paraquat and copper, and also by fenpropimorph, a sterol biosynthesis inhibitor (SBI) fungicide. These results suggest that GintSOD1 is involved in the detoxification of ROS generated from metabolic processes and by external agents. In particular, our data indicate that the antifungal effects of fenpropimorph might not be only due to the interference with sterol metabolism but also to the perturbation of other biological processes and that ROS production and scavenging systems are involved in the response to SBI fungicides.

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Section: Introductionmentioning

confidence: 99%

Characterization of a CuZn superoxide dismutase gene in the arbuscular mycorrhizal fungus Glomus intraradices

et al. 2010

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“…Diverse studies have shown that apoptotic cells can be a source of ROS, and therefore of oxidative damage (Perrone et al, 2008). Consequently, we determined protein carbonylation in aif1 cells after 24 h of selenite treatment, compared with wild-type cells.…”

Section: Selenite Provokes An Increase Of Protein Carbonylationmentioning

confidence: 99%

“…Oxidative stress is among the apoptosis inducers in yeast (Perrone et al, 2008). Thus, hydrogen peroxide at low concentrations provokes apoptosis in a process dependent on the metacaspase Yca1p and on a functional mitochondrial respiratory chain, while high peroxide concentrations provoke non-apoptotic death (Khan et al, 2005;Madeo et al, 1999Madeo et al, , 2002.…”

Section: Introductionmentioning

confidence: 99%

Selenite-induced cell death in Saccharomyces cerevisiae: protective role of glutaredoxins

2010

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Unlike in 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 growing under fermentative metabolism, its effects can be dissected into two death phases. From the time of initial treatment, it causes loss of membrane integrity and genotoxicity. Both effects occur at higher levels in mutants lacking Grx1p and Grx2p than in wild-type cells, and are reversed by expression of a cytosolic version of the membrane-associated Grx7p glutaredoxin. Grx7p can also rescue the high levels of protein carbonylation damage that occur in selenite-treated cultures of the grx1 grx2 mutant. After longer incubation times, selenite causes abnormal nuclear morphology and the appearance of TUNELpositive cells, which are considered apoptotic markers in yeast cells. This effect is independent of Grx1p and Grx2p. Therefore, the protective role of the two glutaredoxins is restricted to the initial stages of selenite treatment. Lack of Yca1p metacaspase or of a functional mitochondrial electron transport chain only moderately diminishes apoptotic-like death by selenite. In contrast, seleniteinduced apoptosis is dependent on the apoptosis-inducing factor Aif1p. In the absence of the latter, intracellular protein carbonylation is reduced after prolonged selenite treatment, supporting the supposition that part of the oxidative damage is contributed by apoptotic cells. INTRODUCTIONSelenium (Se) is a trace element which may have anticarcinogenic action at low concentrations (Letavayová et al., 2006). The essential character of Se in the mammalian diet is related to its presence as selenocysteine in a number of selenoproteins, such as thioredoxin reductases and glutathione peroxidases (Lu & Holmgren, 2009). These enzymes act in the defence against oxidative stress. In contrast, at high concentrations, Se is toxic because it generates oxidative stress and provokes DNA damage (Hatfield et al., 2006;Letavayová et al., 2006). Among the Se compounds that may come into contact with cells, selenite is a prooxidant because it undergoes glutathionemediated reduction to hydrogen selenide with the subsequent formation of superoxide radicals, which can undergo conversion into other reactive oxygen species (ROS) Spallholz, 1997;Tarze et al., 2007). Saccharomyces cerevisiae is a suitable organism to study the toxic properties of Se and the cellular mechanisms which prevent or repair its effects, without the interference due to an Se requirement for selenoproteins. In fact, S. cerevisiae, and fungi in general, do not contain selenoproteins and therefore Se is not essential for these organisms (Lu & Holmgren, 2009). High concentrations of Se cause DNA double-strand breaks in exponentially growing S. cerevisiae cells (Letavayová et al., 2008) and RAD9-dependent cell cycle arrest (Pinson et al., 2000). Accordingly, yeast mutants defective in the RAD9-mediated DNA repair pathway or the RAD6/RAD...

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“…Further investigation of the molecular mechanisms involved in this process showed that a chronic decrease in ATP/ADP⅐P i ratio induced an increase in the intracellular glutathione redox state. Cellular mechanisms that maintain redox homeostasis are crucial, because they provide a buffer against conditions that may perturb the redox environment of cells and/or induce oxidative stress (36,39,40). The abundance of glutathione (1-10 mM) in cells and its low redox potential (Ϫ240 mV) make the glutathione system a major intracellular redox buffer in most cells (36,41,42).…”

Section: Discussionmentioning

confidence: 99%

cAMP-induced Mitochondrial Compartment Biogenesis

Yoboue

Augier

Galinier

et al. 2012

Journal of Biological Chemistry

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Background: Mitochondrial biogenesis is a complex process, and its regulation is not well known. Results: cAMP-induced mitochondrial biogenesis through a decrease in the cellular phosphate potential is due to an increase in the glutathione redox status. Conclusion: Mitochondrial biogenesis is tightly linked to glutathione redox status. Significance: This is the first evidence for a glutathione redox control of a transcription factor involved in mitochondrial biogenesis.

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Reactive oxygen species and yeast apoptosis

Cited by 353 publications

References 172 publications

Characterization of a CuZn superoxide dismutase gene in the arbuscular mycorrhizal fungus Glomus intraradices

Characterization of a CuZn superoxide dismutase gene in the arbuscular mycorrhizal fungus Glomus intraradices

Selenite-induced cell death in Saccharomyces cerevisiae: protective role of glutaredoxins

cAMP-induced Mitochondrial Compartment Biogenesis

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