Resveratrol induces antioxidant defence via transcription factor Yap1p

Escoté, Xavier; Miranda, Merce; Menoyo, Sandra; Rodríguez-Porrata, Boris; Carmona-Gutiérrez, Didac; Jungwirth, Helmut; Madeo, Frank; Cordero, Ricardo; Mas, Albert; Tinahones, Francisco J.; Clotet, Josep; Vendrell, Joan

doi:10.1002/yea.2903

Cited by 31 publications

(27 citation statements)

References 34 publications

(41 reference statements)

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“…Thus, the negative-oxygen consumption values reported in the present study could be associated with an increase in O 2 concentration in the medium as a result of the reactions by superoxide dismutase on O 2 .-(McCord and Fridovich 1969) and subsequent activity of catalase on H 2 O 2 (George 1947). In agreement with this observation, has been reported that RSV acts as a pro-oxidant molecule in S. cerevisiae (Escote et al 2012). Altogether, these findings support the hypothesis that RSV inhibits respiration generating a negative energy status of the cell with a subsequent stimulation of glycolysis to compensate the energy state.…”

Section: Discussionsupporting

confidence: 91%

Resveratrol increases glycolytic flux in Saccharomyces cerevisiae via a SNF1-dependet mechanism

Madrigal‐Perez

Nava

González‐Hernández

et al. 2015

J Bioenerg Biomembr

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Evidence suggests that AMP protein kinase (AMPK) is the main target of the phytochemical resveratrol (RSV) in mammalian cells. Data also indicates that RSV stimulates glucose metabolism; however, the molecular link between RSV and glucose uptake remains unknown. Herein, we provide evidence indicating that RSV stimulates glycolysis via sucrose non-fermenting 1 gene (SNF1, Saccharomyces cerevisiae orthologous of AMPK). S. cerevisiae cultures treated with 30 μM RSV showed an increase in extracellular acidification rate compared to untreated cells, indicating an elevated glycolytic flux. Also, RSV treatment increased transcription levels of two key glycolytic genes, hexokinase 2 (HXK2) and phosphofructokinase 1 (PFK1), as well as production of NADH. Moreover, RSV treatment inhibited mitochondrial respiration when glucose was used as a carbon source. Importantly, the effects of RSV on glycolysis were dependent of SNF1. Taken together, these findings suggest that SNF1 (AMPK in mammalian systems) is the molecular target of RSV in S. cerevisiae.

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Section: Discussionsupporting

confidence: 91%

Resveratrol increases glycolytic flux in Saccharomyces cerevisiae via a SNF1-dependet mechanism

Madrigal‐Perez

Nava

González‐Hernández

et al. 2015

J Bioenerg Biomembr

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“…This increase in ROS following resveratrol treatment has been seen previously in yeast cells 24 , human adipocytes 24 , and cancer cell-lines 25 . In addition, the increase in ROS following preconditioning treatments is a well observed phenomenon, and inhibition of ROS production has been shown to ameliorate preconditioning-induced neuroprotective effects 26 .…”

Section: Discussionsupporting

confidence: 81%

Resveratrol Preconditioning Protects Against Cerebral Ischemic Injury via Nuclear Erythroid 2–Related Factor 2

Narayanan

Dave

Saul

et al. 2015

Stroke

111

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Background and Purpose-Nuclear erythroid 2 related factor 2 (Nrf2) is an astrocyte-enriched transcription factor that has previously been shown to upregulate cellular antioxidant systems in response to ischemia. Although resveratrol preconditioning (RPC) has emerged as a potential neuroprotective therapy, the involvement of Nrf2 in RPC-induced neuroprotection and mitochondrial reactive oxygen species production after cerebral ischemia remains unclear. The goal of our study was to study the contribution of Nrf2 to RPC and its effects on mitochondrial function. Methods-We used rodent astrocyte cultures and an in vivo stroke model with RPC. An Nrf2 DNA binding ELISA and protein analysis via Western blotting of downstream Nrf2 targets were performed to determine RPC-induced activation of Nrf2 in rat and mouse astrocytes. After RPC, mitochondrial function was determined by measuring reactive oxygen species production and mitochondrial respiration in both wild-type and Nrf2 −/− mice. Infarct volume was measured to determine neuroprotection, whereas protein levels were measured by immunoblotting. Results-We report that Nrf2 is activated by RPC in rodent astrocyte cultures, and that loss of Nrf2 reduced RPC-mediated neuroprotection in a mouse model of focal cerebral ischemia. In addition, we observed that wild-type and Nrf2 −/− cortical mitochondria exhibited increased uncoupling and reactive oxygen species production after RPC treatments. Finally, Nrf2 −/− astrocytes exhibited decreased mitochondrial antioxidant expression and were unable to upregulate cellular antioxidants after RPC treatment. Conclusions-Nrf2

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“…The effect of MEL on S. cerevisiae may also be comparable to the effect of resveratrol on yeast (Escoté et al, 2012), which induces Yap1p activity (the major regulator of genes involved in the oxidative stress response) to reduce ROS levels under oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Melatonin Reduces Oxidative Stress Damage Induced by Hydrogen Peroxide in Saccharomyces cerevisiae

Vázquez¹,

González²,

Sempere³

et al. 2017

Front. Microbiol.

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Melatonin (N-acetyl-5-methoxytryptamine), which is synthesized from tryptophan, is formed during alcoholic fermentation, though its role in yeast is unknown. This study employed Saccharomyces cerevisiae as an eukaryote model to evaluate the possible effects of melatonin supplementation on endogenous cellular defense systems by measuring its effects on various cellular targets. Cell viability, intracellular reduced and oxidized glutathione levels (GSH and GSSG, respectively), reactive oxygen species (ROS) production, and expression of genes related to antioxidant defense in yeast, such as the glutathione system, catalase, superoxide dismutase, glutaredoxin, and thioredoxin, were assessed. Melatonin alone decreased GSH, increased GSSG, and activated antioxidant defense system genes, which reached maximum levels in the stationary phase. These results indicate that melatonin supplementation enables cells to resist better the stress generated in the stationary phase. However, when cells were subjected to oxidative stress induced by H2O2, melatonin was able to partially mitigate cell damage by decreasing ROS accumulation and GSH and increasing GSSG; this was followed by enhanced cell viability after stress exposure, mostly when occurring in the early stationary phase. Additionally, under such conditions, most genes related to endogenous antioxidant defense continued to be up-regulated with melatonin supplementation. The findings demonstrate that melatonin can act as antioxidant in S. cerevisiae.

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Resveratrol induces antioxidant defence via transcription factor Yap1p

Cited by 31 publications

References 34 publications

Resveratrol increases glycolytic flux in Saccharomyces cerevisiae via a SNF1-dependet mechanism

Resveratrol increases glycolytic flux in Saccharomyces cerevisiae via a SNF1-dependet mechanism

Resveratrol Preconditioning Protects Against Cerebral Ischemic Injury via Nuclear Erythroid 2–Related Factor 2

Melatonin Reduces Oxidative Stress Damage Induced by Hydrogen Peroxide in Saccharomyces cerevisiae

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