ArticleToxicological sciences : an official journal of the Society of Toxicology2008
Comparative induction of 28S ribosomal RNA cleavage by ricin and the trichothecenes deoxynivalenol and T-2 toxin in the macrophage.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 76 citations in OpenAlex.
- A human cell-free translation screen identifies the NT-2 mycotoxin as a ribosomal inhibitor that binds the peptidyl transferase center.Communications biology · 2026Article
- Impacts of trichothecene mycotoxins on human colonic epithelial cells: molecular mechanisms and signaling pathways.Journal of advanced research · 2026Review
- Direct T-2 Toxicity on Human Skin-Fibroblast Hs68 Cell Line-In Vitro Study.International journal of molecular sciences · 2022Article
- Article
- A Quick Guide to Small-Molecule Inhibitors of Eukaryotic Protein Synthesis.Biochemistry. Biokhimiia · 2020Review
- Mycotoxin Deoxynivalenol Has Different Impacts on Intestinal Barrier and Stem Cells by Its Route of Exposure.Toxins · 2020Article
- Deoxynivalenol Exposure Suppresses Adipogenesis by Inhibiting the Expression of Peroxisome Proliferator-Activated Receptor Gamma 2 (PPARγ2) in 3T3-L1 Cells.International journal of molecular sciences · 2020Article
- The food contaminant deoxynivalenol provokes metabolic impairments resulting in non-alcoholic fatty liver (NAFL) in mice.Scientific reports · 2020Article
- Article
- Review
- Whole-Cell Multiparameter Assay for Ricin and Abrin Activity-Based Digital Holographic Microscopy.Toxins · 2019Article
- Saccharomyces cerevisiae Boulardii Reduces the Deoxynivalenol-Induced Alteration of the Intestinal Transcriptome.Toxins · 2018Article
- Article
- Intestinal toxicity of the type B trichothecene mycotoxin fusarenon-X: whole transcriptome profiling reveals new signaling pathways.Scientific reports · 2017Article
- T-2 mycotoxin: toxicological effects and decontamination strategies.Oncotarget · 2017Review
- Article
- Ribosomal alteration-derived signals for cytokine induction in mucosal and systemic inflammation: noncanonical pathways by ribosomal inactivation.Mediators of inflammation · 2014Review
- Mechanisms for ribotoxin-induced ribosomal RNA cleavage.Toxicology and applied pharmacology · 2012Article
- Targets and intracellular signaling mechanisms for deoxynivalenol-induced ribosomal RNA cleavage.Toxicological sciences : an official journal of the Society of Toxicology · 2012Article
- Aberrant expression of miR-638 contributes to benzo(a)pyrene-induced human cell transformation.Toxicological sciences : an official journal of the Society of Toxicology · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
Ribosome-inactivating proteins (RIPs) and sesquiterpenoid trichothecene mycotoxins are known to bind to eukaryotic ribosomes, inhibit translation and activate mitogen-activated protein kinases. Here we compared the capacities of the RIP ricin to promote 28S ribosomal RNA (rRNA) cleavage with that of the trichothecenes, deoxynivalenol (DON), and T-2 toxin (T-2). In a cell-free model, exposure to ricin at 300 ng/ml for 30 min depurinated yeast 28S rRNA, however, neither DON (< or = 4 microg/ml) nor T-2 (< or = 2 microg/ml) exhibited this N-glycosidase activity. Incubation of RAW 264.7 macrophages with ricin (20-320 ng/ml), DON (250-5000 ng/ml), or T-2 (2-80 ng/ml) for 6 h, however, generated 28S rRNA-specific products consistent with cleavage sites near the 3' terminal end of murine 28S rRNA. Oligonucleotide extension analysis of treated RAW 264.7 cells revealed that ricin evoked 28S rRNA damage at one site in the alpha-sarcin/ricin (S/R)-loop (A4256) and two other sites (A3560 and A4045) in the peptidyl transferase center. Although DON or T-2 did not damage the S/R loop, these trichothecenes did promote cleavage at A3560 and A4045. In addition, incubation of the cells with ricin (> or = 20 ng/ml), DON (> or = 250 ng/ml), or T-2 (> or = 10 ng/ml) induced RNase activity as well as RNase L mRNA and protein expression. These data suggest that only ricin directly damaged 28S rRNA under cell-free conditions but that ricin, DON, and T-2 promoted intracellular 28S rRNA cleavage, potentially by facilitating the action of endogenous RNases and/or by upregulating RNase expression.
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