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Ribosome quality control is a central protection mechanism for yeast exposed to Deoxynivalenol and Trichothecin

ABSTRACT: Trichothecenes, like deoxynivalenol (DON) are secondary metabolites of Fusarium species, and are major pollutants in cereal food and feed products. They inhibit eukaryotic protein synthesis, however with only partly resolved consequences for the cellular homeostasis. Here we report a systematic functional investigation of the effects of DON on exponential phase growing yeast cells using either short doses of DON or continuos treatment with DON.

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE75462 | GEO | 2016/06/03

SECONDARY ACCESSION(S): PRJNA304351

REPOSITORIES: GEO

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Deoxynivalenol affects the gene expression of A549 lung epithelial cells

Project description:Deoxynivalenol (DON) is an important Fusarium toxin of concern for food safety. The inhalation of powder contaminated with deoxynivalenol is possible and may cause lung toxicity. In this study, we investigated the gene expression profile of A549 cells treated with 0.2 microg/mL deoxynivalenol by microarray analysis. In total, 16 genes and 5 noncoding RNAs were significantly affected by deoxynivalenol treatment. 4 samples; 2 samples from nontreated cells and other 2 samples from 0.2 microg/mL DON-treated cells for 24 hours

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Deoxynivalenol affects the gene expression of A549 lung epithelial cells

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Transcriptome analysis of Escherichia coli under deoxynivalenol and nivalenol conditions

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Project description:Deoxynivalenol (DON), 3-acetyldeoxynivalenol (3-ADON) and 15-acetyldeoxynivalenol (15-ADON) are type B trichothecenes and are major pollutants in food and feed products. Although the toxicity of DON has been well documented, the information of toxicity of its acetylated derivative remains incomplete. To acquire more detailed insight in 3-ADON and 15-ADON, Caco-2 cells under 0.5 µM DON, 3-ADON and 15-ADON treatment for 24 h were subjected to RNA-seq analysis. In the present study, 2656, 3132 and 2425 differentially expressed genes (DEGs) were selected respectively and were enriched utilizing KEGG and GO database. The upregulation of ataxia-telangiectasia mutated kinase (ATM), WEE1 homolog 2 (WEE2) and downregulation of proliferating cell nuclear antigen (PCNA), minichromosome maintenance (MCMs), cyclin dependent kinase (CDKs), E2Fs indicate that the three toxins induced DNA damage, inhibition of DNA replication and cell cycle arrest in Caco-2 cells. Apart from these, the upregulation of sestrin (SENEs) and NEIL1 implied that the reason of DNA damage may attribute to oxidative stress. Our study provides an insight in the toxic mechanism of 3-ADON and 15-ADON.

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2011-11-05 | E-GEOD-25185 | biostudies-arrayexpress

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