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Toxins 2016, 8(8), 232; doi:10.3390/toxins8080232

Hydrolytic Fate of 3/15-Acetyldeoxynivalenol in Humans: Specific Deacetylation by the Small Intestine and Liver Revealed Using in Vitro and ex Vivo Approaches

1
Aix Marseille Univ, CNRS, Centrale Marseille, iSm2, Marseille, France
2
Aix Marseille Univ, Laboratoire de Biomécanique Appliquée, UMRT24 IFSTTAR, Faculté de médecine secteur Nord, Boulevard Pierre Dramard, F-13916 Marseille Cedex 20, France
3
Aix Marseille Univ, CNRS, CRN2M, Marseille, France & CSO@MyEnterix, Marseille, France
*
Author to whom correspondence should be addressed.
Academic Editor: Carlo Brera
Received: 19 June 2016 / Accepted: 19 July 2016 / Published: 28 July 2016
(This article belongs to the Special Issue Exposure and Risk Assessment for Mycotoxins)
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Abstract

In addition to deoxynivalenol (DON), acetylated derivatives, i.e., 3-acetyl and 15-acetyldexynivalenol (or 3/15ADON), are present in cereals leading to exposure to these mycotoxins. Animal and human studies suggest that 3/15ADON are converted into DON after their ingestion through hydrolysis of the acetyl moiety, the site(s) of such deacetylation being still uncharacterized. We used in vitro and ex vivo approaches to study the deacetylation of 3/15ADON by enzymes and cells/tissues present on their way from the food matrix to the blood in humans. We found that luminal deacetylation by digestive enzymes and bacteria is limited. Using human cells, tissues and S9 fractions, we were able to demonstrate that small intestine and liver possess strong deacetylation capacity compared to colon and kidneys. Interestingly, in most cases, deacetylation was more efficient for 3ADON than 15ADON. Although we initially thought that carboxylesterases (CES) could be responsible for the deacetylation of 3/15ADON, the use of pure human CES1/2 and of CES inhibitor demonstrated that CES are not involved. Taken together, our original model system allowed us to identify the small intestine and the liver as the main site of deacetylation of ingested 3/15ADON in humans. View Full-Text
Keywords: mycotoxin; deoxynivalenol; 3-acetyldeoxynivalenol; 15-acetyldeoxynivalenol; carboxylesterase; human explants; Caco-2; T84; HepG2; A498 mycotoxin; deoxynivalenol; 3-acetyldeoxynivalenol; 15-acetyldeoxynivalenol; carboxylesterase; human explants; Caco-2; T84; HepG2; A498
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Ajandouz, E.H.; Berdah, S.; Moutardier, V.; Bege, T.; Birnbaum, D.J.; Perrier, J.; Di Pasquale, E.; Maresca, M. Hydrolytic Fate of 3/15-Acetyldeoxynivalenol in Humans: Specific Deacetylation by the Small Intestine and Liver Revealed Using in Vitro and ex Vivo Approaches. Toxins 2016, 8, 232.

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