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Calcium-Sensing Receptor and Transient Receptor Ankyrin-1 Mediate Emesis Induction by Deoxynivalenol (Vomitoxin).
Wu, Wenda; Zhou, Hui-Ren; Bursian, Steven J; Link, Jane E; Pestka, James J.
Afiliación
  • Wu W; College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, People's Republic of China.
  • Zhou HR; Department of Food Science and Human Nutrition, Michigan State University, East Lansing, Michigan 48824.
  • Bursian SJ; Department of Food Science and Human Nutrition, Michigan State University, East Lansing, Michigan 48824.
  • Link JE; Center for Integrative Toxicology, Michigan State University, East Lansing, Michigan 48824.
  • Pestka JJ; Department of Animal Science, Michigan State University, East Lansing, Michigan 48824.
Toxicol Sci ; 155(1): 32-42, 2017 01.
Article en En | MEDLINE | ID: mdl-27667315
The common foodborne mycotoxin deoxynivalenol (DON, vomitoxin) can negatively impact animal and human health by causing food refusal and vomiting. Gut enteroendocrine cells (EECs) secrete hormones that mediate DON's anorectic and emetic effects. In prior work utilizing a cloned EEC model, our laboratory discovered that DON-induced activation of calcium-sensing receptor (CaSR), a G-coupled protein receptor (GPCR), and transient receptor ankyrin-1 (TRPA1), a transient receptor potential (TRP) channel, drives Ca2+-mediated hormone secretion. Consistent with these in vitro findings, CaSR and TRPA1 mediate DON-induced satiety hormone release and food refusal in the mouse, an animal model incapable of vomiting. However, the roles of this GPCR and TRP in DON's emetic effects remain to be determined. To address this, we tested the hypothesis that DON triggers emesis in mink by activating CaSR and TRPA1. Oral gavage with selective agonists for CaSR (R-568) or TRPA1 (allyl isothiocyanate; AITC) rapidly elicited emesis in the mink in dose-dependent fashion. Oral pretreatment of the animals with the CaSR antagonist NPS-2143 or the TRP antagonist ruthenium red (RR), respectively, inhibited these responses. Importantly, DON-induced emesis in mink was similarly inhibited by oral pretreatment with NPS-2143 or RR. In addition, these antagonists suppressed concurrent DON-induced elevations in plasma peptide YY3-36 and 5-hydroxytryptamine-hormones previously demonstrated to mediate the toxin's emetic effects in mink. Furthermore, antagonist co-treatment additively suppressed DON-induced emesis and peptide YY 3-36 release. To summarize, the observations here strongly suggest that activation of CaSR and TRPA1 might have critical roles in DON-induced emesis.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Tricotecenos / Vómitos / Ancirinas / Receptores Sensibles al Calcio Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Toxicol Sci Asunto de la revista: TOXICOLOGIA Año: 2017 Tipo del documento: Article Pais de publicación: Estados Unidos
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Tricotecenos / Vómitos / Ancirinas / Receptores Sensibles al Calcio Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Toxicol Sci Asunto de la revista: TOXICOLOGIA Año: 2017 Tipo del documento: Article Pais de publicación: Estados Unidos