Acrolein toxicity involves oxidative stress caused by glutathione depletion in the yeast Saccharomyces cerevisiae

Kwolek‐Mirek, Magdalena; Bednarska, Sabina; Bartosz, Grzegorz; Biliński, T

doi:10.1007/s10565-008-9090-x

Cited by 30 publications

(36 citation statements)

References 33 publications

(45 reference statements)

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“…Although this was not detected during conidiation, during growth A. nidulans Δ napA mutants show a decreased GSH/GSSG ratio and a 1.6 fold decrease in total glutathione content when compared to a WT strain (Thön et al, 2010). This is consistent with the fact that Δ napA mutants are very sensitive to AA/acrolein, known to cause GSH depletion (Kwolek-Mirek et al, 2009). Such a decrease in reducing power might provide additional difficulties in catabolizing carbon sources that are more demanding on these resources.…”

Section: Discussionsupporting

confidence: 86%

“…However, the Δ napA mutant was also unable to grow on glucose plus AA (Figures 8A,B). AA/acrolein causes oxidative stress and induces Yap1 activation in S. cerevisiae (Kwolek-Mirek et al, 2009; Golla et al, 2015) and therefore it might result particularly toxic for the Δ napA mutant. To test this, we generated Δ alcA and Δ napA Δ alcA mutants and examined them for ethanol utilization and AA resistance.…”

Section: Resultsmentioning

confidence: 99%

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NapA Mediates a Redox Regulation of the Antioxidant Response, Carbon Utilization and Development in Aspergillus nidulans

Mendoza-Martínez¹,

Lara-Rojas²,

Sánchez³

et al. 2017

Front. Microbiol.

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The redox-regulated transcription factors (TFs) of the bZIP AP1 family, such as yeast Yap1 and fission yeast Pap1, are activated by peroxiredoxin proteins (Prxs) to regulate the antioxidant response. Previously, Aspergillus nidulans mutants lacking the Yap1 ortholog NapA have been characterized as sensitive to H2O2 and menadione. Here we study NapA roles in relation to TFs SrrA and AtfA, also involved in oxidant detoxification, showing that these TFs play different roles in oxidative stress resistance, catalase gene regulation and development, during A. nidulans life cycle. We also uncover novel NapA roles in repression of sexual development, normal conidiation, conidial mRNA accumulation, and carbon utilization. The phenotypic characterization of ΔgpxA, ΔtpxA, and ΔtpxB single, double and triple peroxiredoxin mutants in wild type or ΔnapA backgrounds shows that none of these Prxs is required for NapA function in H2O2 and menadione resistance. However, these Prxs participate in a minor NapA-independent H2O2 resistance pathway and NapA and TpxA appear to regulate conidiation along the same route. Using transcriptomic analysis we show that during conidial development NapA-dependent gene expression pattern is different from canonical oxidative stress patterns. In the course of conidiation, NapA is required for regulation of at least 214 genes, including ethanol utilization genes alcR, alcA and aldA, and large sets of genes encoding proteins involved in transcriptional regulation, drug detoxification, carbohydrate utilization and secondary metabolism, comprising multiple oxidoreductases, membrane transporters and hydrolases. In agreement with this, ΔnapA mutants fail to grow or grow very poorly in ethanol, arabinose or fructose as sole carbon sources. Moreover, we show that NapA nuclear localization is induced not only by oxidative stress but also by growth in ethanol and by carbon starvation. Together with our previous work, these results show that SakA-AtfA, SrrA and NapA oxidative stress-sensing pathways regulate essential aspects of spore physiology (i.e., cell cycle arrest, dormancy, drug production and detoxification, and carbohydrate utilization).

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Section: Discussionsupporting

confidence: 86%

Section: Resultsmentioning

confidence: 99%

NapA Mediates a Redox Regulation of the Antioxidant Response, Carbon Utilization and Development in Aspergillus nidulans

Mendoza-Martínez¹,

Lara-Rojas²,

Sánchez³

et al. 2017

Front. Microbiol.

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“…61 These results fit into a pattern suggested by the results of others. Glutathione depletion is associated with oxidative stress and toxicity from hydrogen peroxide (H 2 O 2 ) 62 as well as from acrolein, 63 but acrolein toxicity has been shown to be more severe than that of H 2 O 2 . 35 Subtoxic levels of oxidative stress due to H 2 O 2 induce senescence in RPE cells via TGFβ2 release 13 which can directly upregulate VEGF by ARPE-19 cells 14 and RPE primary cultures via mitogen-associated protein kinases, 9 as well as JNK, PI3K, NF-κB, and others.…”

Section: Discussionmentioning

confidence: 99%

NBHA Reduces Acrolein-Induced Changes in ARPE-19 Cells: Possible Involvement of TGFβ

Vidro-Kotchan

Yendluri

Tsin

2011

Current Eye Research

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Purpose Acrolein, a toxic, reactive aldehyde formed metabolically and environmentally, has been implicated in the damage to and dysfunction of the retinal pigment epithelium (RPE) that accompanies age-related macular degeneration (AMD). Our purpose was to investigate the potential of acrolein to influence the release of transforming growth factor beta-2 (TGFβ2) and vascular endothelial growth factor (VEGF), to assess the ability of N-benzylhydroxylamine (NBHA) to prevent the effect of acrolein on cytokine release and reduction of viable cells, and to explore the pathway by which acrolein might be causing the increase of VEGF. Materials and Methods Confluent ARPE-19 cells were treated with acrolein and/or NBHA. They were also pretreated with SIS3, a specific inhibitor of SMAD 3, and ZM39923, a JAK3 inhibitor, before being treated with acrolein. Viable cells were counted; ELISA was used to measure the TGFβ2 and/or VEGF in the conditioned media. Results Acrolein was shown to reduce the number of viable ARPE-19 cells and to upregulate the release of the proangiogenic cytokines TGFβ2 and VEGF. Co-treatment with 200 μM NBHA significantly reduced the effects of acrolein on viable cell number and TGFβ2 release. Pretreatment of the cells with SIS3 partially blocked the action of acrolein on decreased viable cell number and VEGF upregulation, suggesting that part of the effects of acrolein are mediated by the increased levels of TGFβ and its signaling. Conclusions Our results suggest that the action of acrolein on the reduction of viability and VEGF increase by ARPE-19 cells is partially mediated by TGFβ2. By reducing the effects of acrolein, NBHA and SIS3 could be potential pharmacological agents in the prevention and progression of acrolein-induced damage to the RPE that relates to AMD.

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“…We performed a calibration curve using 1,1,3,3-tetramethoxypropane 500 μM as standard. The results were expressed as micromoles of TBARS by 5× 10 8 cells (Kwolek-Mirek et al , 2009). The concentrations were determined in triplicate for each sample.…”

Section: Methodsmentioning

confidence: 99%

Biomarkers to evaluate the effects of temperature and methanol on recombinant Pichia pastoris

Zepeda

Figueroa

Abdalla

et al. 2014

Braz. J. Microbiol.

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Pichia pastoris is methylotrophic yeast used as an efficient expression system for heterologous protein production. In order to evaluate the effects of temperature (10 and 30 °C) and methanol (1 and 3% (v/v)) on genetically-modified Pichia pastoris, different biomarkers were evaluated: Heat stress (HSF-1 and Hsp70), oxidative stress (OGG1 and TBARS) and antioxidant (GLR). Three yeast cultures were performed: 3X = 3% methanol-10 °C, 4X = 3% methanol-30 °C, and 5X = 1% methanol-10°C. The expression level of HIF-1α, HSF-1, HSP-70 and HSP-90 biomarkers were measured by Western blot and in situ detection was performed by immunocytochemistry. Ours results show that at 3% methanol −30 °C there is an increase of mitochondrial OGG1 (mtOGG1), Glutathione Reductase (GLR) and TBARS. In addition, there was a cytosolic expression of HSF-1 and HSP-70, which indicates a deprotection against nucleolar fragmentation (apoptosis). On the other hand, at 3% methanol −10 °C and 1% and at methanol −10 °C conditions there was nuclear expression of OGG1, lower levels of TBARS and lower expression of GLR, cytosolic expression of HSF-1 and nuclear expression HSP-70. In conclusion, our results suggest that 3% methanol-30 °C is a condition that induces a strong oxidative stress and risk factors of apoptosis in modified-genetically P. pastoris.

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Acrolein toxicity involves oxidative stress caused by glutathione depletion in the yeast Saccharomyces cerevisiae

Cited by 30 publications

References 33 publications

NapA Mediates a Redox Regulation of the Antioxidant Response, Carbon Utilization and Development in Aspergillus nidulans

NapA Mediates a Redox Regulation of the Antioxidant Response, Carbon Utilization and Development in Aspergillus nidulans

NBHA Reduces Acrolein-Induced Changes in ARPE-19 Cells: Possible Involvement of TGFβ

Biomarkers to evaluate the effects of temperature and methanol on recombinant Pichia pastoris

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