ArticleToxicological sciences : an official journal of the Society of Toxicology2014
Comparison of anorectic and emetic potencies of deoxynivalenol (vomitoxin) to the plant metabolite deoxynivalenol-3-glucoside and synthetic deoxynivalenol derivatives EN139528 and EN139544.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 43 citations in OpenAlex.
- Review
- Hazard characterisation for significant mycotoxins in food.Mycotoxin research · 2023Review
- Neither GLP-1 receptors nor GFRAL neurons are required for aversive or anorectic response to DON (vomitoxin).American journal of physiology. Regulatory, integrative and comparative physiology · 2023Article
- Review
- Substance P and Glucagon-like Peptide-1Toxins · 2022Article
- Article
- Deoxynivalenol (Vomitoxin)-Induced Anorexia Is Induced by the Release of Intestinal Hormones in Mice.Toxins · 2021Article
- COVID-19, nausea, and vomiting.Journal of gastroenterology and hepatology · 2021Review
- The mycotoxin deoxynivalenol activates GABAergic neurons in the reward system and inhibits feeding and maternal behaviours.Archives of toxicology · 2020Article
- Type A Trichothecene Diacetoxyscirpenol-Induced Emesis Corresponds to Secretion of Peptide YY and Serotonin in Mink.Toxins · 2020Article
- Microbiological quality of mink feed raw materials and feed production area.Acta veterinaria Scandinavica · 2019Article
- Risks to human and animal health related to the presence of deoxynivalenol and its acetylated and modified forms in food and feed.EFSA journal. European Food Safety Authority · 2017Article
- Review
- Calcium-Sensing Receptor and Transient Receptor Ankyrin-1 Mediate Emesis Induction by Deoxynivalenol (Vomitoxin).Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- Modeling the emetic potencies of food-borne trichothecenes by benchmark dose methodology.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2016Article
- Emetic responses to T-2 toxin, HT-2 toxin and emetine correspond to plasma elevations of peptide YY3-36 and 5-hydroxytryptamine.Archives of toxicology · 2016Article
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Authors and funding
10 authors at 3 institutions in 4 countries.
Funding
Abstract
The mycotoxin deoxynivalenol (DON) elicits robust anorectic and emetic effects in several animal species. However, less is known about the potential for naturally occurring and synthetic congeners of this trichothecene to cause analogous responses. Here we tested the hypothesis that alterations in DON structure found in the plant metabolite deoxynivalenol-3-glucoside (D3G) and two pharmacologically active synthetic DON derivatives, EN139528 and EN139544, differentially impact their potential to evoke food refusal and emesis. In a nocturnal mouse food consumption model, oral administration with DON, D3G, EN139528, or EN139544 at doses from 2.5 to 10 mg/kg BW induced anorectic responses that lasted up to 16, 6, 6, and 3 h, respectively. Anorectic potency rank orders were EN139544>DON>EN139528>D3G from 0 to 0.5 h but DON>D3G>EN139528>EN139544 from 0 to 3 h. Oral exposure to each of the four compounds at a common dose (2.5 mg/kg BW) stimulated plasma elevations of the gut satiety peptides cholecystokinin and to a lesser extent, peptide YY3-36 that corresponded to reduced food consumption. In a mink emesis model, oral administration of increasing doses of the congeners differentially induced emesis, causing marked decreases in latency to emesis with corresponding increases in both the duration and number of emetic events. The minimum emetic doses for DON, EN139528, D3G, and EN139544 were 0.05, 0.5, 2, and 5 mg/kg BW, respectively. Taken together, the results suggest that although all three DON congeners elicited anorectic responses that mimicked DON over a narrow dose range, they were markedly less potent than the parent mycotoxin at inducing emesis.
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