ArticleToxicological sciences : an official journal of the Society of Toxicology2013
Peptide YY3-36 and 5-hydroxytryptamine mediate emesis induction by trichothecene deoxynivalenol (vomitoxin).
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 62 citations in OpenAlex.
- Neurotoxicological Effects of Some Mycotoxins on Humans Health and Methods of Neuroprotection.Toxins · 2025Review
- Vitamin 25(OH)DToxins · 2024Article
- Article
- 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
- Assessment of information as regards the toxicity of T-2 and HT-2 toxin for ruminants.EFSA journal. European Food Safety Authority · 2022Article
- Article
- Deoxynivalenol (Vomitoxin)-Induced Anorexia Is Induced by the Release of Intestinal Hormones in Mice.Toxins · 2021Article
- Mechanisms of Nausea and Vomiting: Current Knowledge and Recent Advances in Intracellular Emetic Signaling Systems.International journal of molecular sciences · 2021Review
- Article
- Type A Trichothecene Diacetoxyscirpenol-Induced Emesis Corresponds to Secretion of Peptide YY and Serotonin in Mink.Toxins · 2020Article
- Article
- Article
- Hydrogen-Rich Water and Lactulose Protect Against Growth Suppression and Oxidative Stress in Female Piglets FedToxins · 2018Article
- Article
- 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
- Safety and efficacy of microorganism DSM 11798 as a technological additive for all avian species.EFSA journal. European Food Safety Authority · 2017Article
- 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
- Appropriateness to set a group health based guidance value for T2 and HT2 toxin and its modified forms.EFSA journal. European Food Safety Authority · 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
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Deoxynivalenol (DON, vomitoxin), a trichothecene mycotoxin produced by Fusarium sp. that frequently occurs in cereal grains, has been associated with human and animal food poisoning. Although a common hallmark of DON-induced toxicity is the rapid onset of emesis, the mechanisms for this adverse effect are not fully understood. Recently, our laboratory has demonstrated that the mink (Neovison vison) is a suitable small animal model for investigating trichothecene-induced emesis. The goal of this study was to use this model to determine the roles of two gut satiety hormones, peptide YY3-36 (PYY3-36) and cholecystokinin (CCK), and the neurotransmitter 5-hydroxytryptamine (5-HT) in DON-induced emesis. Following ip exposure to DON at 0.1 and 0.25mg/kg bw, emesis induction ensued within 15-30min and then persisted up to 120min. Plasma DON measurement revealed that this emesis period correlated with the rapid distribution and clearance of the toxin. Significant elevations in both plasma PYY3-36 (30-60min) and 5-HT (60min) but not CCK were observed during emesis. Pretreatment with the neuropeptide Y2 receptor antagonist JNJ-31020028 attenuated DON- and PYY-induced emesis, whereas the CCK1 receptor antagonist devezapide did not alter DON's emetic effects. The 5-HT3 receptor antagonist granisetron completely suppressed induction of vomiting by DON and the 5-HT inducer cisplatin. Granisetron pretreatment also partially blocked PYY3-36-induced emesis, suggesting a potential upstream role for this gut satiety hormone in 5-HT release. Taken together, the results suggest that both PYY3-36 and 5-HT play contributory roles in DON-induced emesis.
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