Decrease of H2O2 Plasma Membrane Permeability during Adaptation to H2O2 in Saccharomyces cerevisiae

Branco, Miguel R.; Marinho, H. Susana; Cyrne, Luísa; Antunes, Fernando

doi:10.1074/jbc.m311818200

Cited by 139 publications

(104 citation statements)

References 39 publications

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“…It has been demonstrated that the deletion of single genes in the ergosterol synthesis pathway rendered yeast cells more susceptible to oxidative stress (Branco et al 2004; Thorpe et al 2004). In addition, H2O2 was found to repress the ergosterol biosynthesis pathway through Pof14, a new member of the Fbox protein family, which binds and decreases the activity of the squalene synthase ERG9, a key enzyme in ergosterol metabolism, leading to a decrease of the total cellular ergosterol levels in Schizosaccharomyces pombe (Tafforeau et al 2006).…”

Section: Discussionmentioning

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: Discussionmentioning

confidence: 99%

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

et al. 2010

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“…H 2 O 2 diffusion across biomembranes is not "free" and gradients are formed when the source of H 2 O 2 is separated from the sink by a biomembrane (33,40 (14,15). In these conditions, cell viability was unaffected (not shown) and p65 translocation was induced significantly, up to 4-fold by H 2 O 2 (Fig.…”

Section: Estimation Of H 2 O 2 Cytosolic Concentrations In Mcf-7 Cellsmentioning

confidence: 95%

A Quantitative Study of NF-κB Activation by H2O2: Relevance in Inflammation and Synergy with TNF-α

Oliveira-Marques

Cyrne

Marinho

et al. 2007

The Journal of Immunology

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112

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Although the germicide role of H2O2 released during inflammation is well established, a hypothetical regulatory function, either promoting or inhibiting inflammation, is still controversial. In particular, after 15 years of highly contradictory results it remains uncertain whether H2O2 by itself activates NF-κB or if it stimulates or inhibits the activation of NF-κB by proinflammatory mediators. We investigated the role of H2O2 in NF-κB activation using, for the first time, a calibrated and controlled method of H2O2 delivery—the steady-state titration—in which cells are exposed to constant, low, and known concentrations of H2O2. This technique contrasts with previously applied techniques, which disrupt cellular redox homeostasis and/or introduce uncertainties in the actual H2O2 concentration to which cells are exposed. In both MCF-7 and HeLa cells, H2O2 at extracellular concentrations up to 25 μM did not induce significantly per se NF-κB translocation to the nucleus, but it stimulated the translocation induced by TNF-α. For higher H2O2 doses this stimulatory role shifts to an inhibition, which may explain published contradictory results. The stimulatory role was confirmed by the observation that 12.5 μM H2O2, a concentration found during inflammation, increased the expression of several proinflammatory NF-κB-dependent genes induced by TNF-α (e.g., IL-8, MCP-1, TLR2, and TNF-α). The same low H2O2 concentration also induced the anti-inflammatory gene coding for heme oxygenase-1 (HO-1) and IL-6. We propose that H2O2 has a fine-tuning regulatory role, comprising both a proinflammatory control loop that increases pathogen removal and an anti-inflammatory control loop, which avoids an exacerbated harmful inflammatory response.

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“…Unlike NO, it appears that cell membranes pose important limiting barriers for the partitioning and diffusion of H 2 O 2 (35)(36)(37). To test this, MCF7 cells were harvested and placed in suspension at various concentrations to increase their density.…”

Section: Hif-1␣ and P53 Regulation By Other Radical/oxidantmentioning

confidence: 99%

Superoxide Fluxes Limit Nitric Oxide-induced Signaling

Thomas

Ridnour

Espey

et al. 2006

Journal of Biological Chemistry

105

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Independently, superoxide (O 2 ؊) and nitric oxide (NO) are biologically important signaling molecules. When co-generated, these radicals react rapidly to form powerful oxidizing and nitrating intermediates. Although this reaction was once thought to be solely cytotoxic, herein we demonstrate using MCF7, macrophage, and endothelial cells that when nanomolar levels of NO and O 2 ؊ were produced concomitantly, the effective NO concentration was established by the relative fluxes of these two radicals. Differential regulation of sGC, pERK, HIF-1␣, and p53 were used as biological dosimeters for NO concentration. Introduction of intracellular-or extracellular-generated O 2 ؊ during NO generation resulted in a concomitant increase in oxidative intermediates with a decrease in steady-state NO concentrations and a proportional reduction in the levels of sGC, ERK, HIF-1␣, and p53 regulation. NO responses were restored by addition of SOD. The intermediates formed from the reactions of NO with O 2 ؊ were non-toxic, did not form 3-nitrotyrosine, nor did they elicit any signal transduction responses. H 2 O 2 in bolus or generated from the dismutation of O 2 ؊ by SOD, was cytotoxic at high concentrations and activated p53 independent of NO. This effect was completely inhibited by catalase, suppressed by NO, and exacerbated by intracellular catalase inhibition. We conclude that the reaction of O 2 ؊ with NO is an important regulatory mechanism, which modulates signaling pathways by limiting steady-state levels of NO and preventing H 2 O 2 formation from O 2 ؊ .

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Decrease of H2O2 Plasma Membrane Permeability during Adaptation to H2O2 in Saccharomyces cerevisiae

Cited by 139 publications

References 39 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

A Quantitative Study of NF-κB Activation by H2O2: Relevance in Inflammation and Synergy with TNF-α

Superoxide Fluxes Limit Nitric Oxide-induced Signaling

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