Metabolism of the masked mycotoxin deoxynivalenol-3-glucoside in pigs

Nagl, Veronika; Woechtl, Bettina; Schwartz-Zimmermann, Heidi E.; Hennig-Pauka, Isabel; Moll, Wulf-Dieter; Adam, Gerhard; Berthiller, Franz

doi:10.1016/j.toxlet.2014.06.032

Cited by 142 publications

(142 citation statements)

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“…These findings correlate well with those of Nagl et al (2012Nagl et al ( , 2014, underlining that the majority of oral administrated D3G was recovered as DON in feces. In vivo, the conversion of D3G to its toxic aglycone may occur in the distal part of the gut, while ingested DON is absorbed in the proximal part of the small intestine (Maresca 2013).…”

Section: Figsupporting

confidence: 82%

“…It has been described that D3G is considerably less bioavailable in mammals when compared to DON. Indeed, following oral administration, only small percentage of applied dose of D3G was found in urine in rats and piglets (Nagl et al 2012(Nagl et al , 2014. Moreover, in a human volunteer consuming a diet naturally contaminated with D3G, the masked mycotoxin could not be detected in urine (Warth et al 2013).…”

Section: Discussionmentioning

confidence: 99%

“…The authors observed that D3G was ineffective in evoking splenic cytokine or chemokine mRNA responses. Because D3G is poorly absorbed, the intestine can be a target for this toxin (De Nijs et al 2012;Nagl et al 2012Nagl et al , 2014.…”

Section: Introductionmentioning

confidence: 99%

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Intestinal toxicity of the masked mycotoxin deoxynivalenol-3-β-d-glucoside

et al. 2015

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Natural food contaminants such as mycotoxins are an important problem for human health. Deoxynivalenol (DON) is one of the most common mycotoxins detected in cereals and grains. Its toxicological effects mainly concern the immune system and the gastrointestinal tract. This toxin is a potent ribotoxic stressor leading to MAP kinase activation and inflammatory response. DON frequently co-occurs with its glucosylated form, the masked mycotoxin deoxynivalenol-3-β-D-glucoside (D3G). The toxicity of this later compound remains unknown in mammals. This study aimed to assess the ability of D3G to elicit a ribotoxic stress and to induce intestinal toxicity. The toxicity of D3G and DON (0-10 µM) was studied in vitro, on the human intestinal Caco-2 cell line, and ex vivo, on porcine jejunal explants. First, an in silico analysis revealed that D3G, contrary to DON, was unable to bind to the A-site of the ribosome peptidyl transferase center, the main targets for DON toxicity. Accordingly, D3G did not activate JNK and P38 MAPKs in treated Caco-2 cells and did not alter viability and barrier function on cells, as measured by the trans-epithelial electrical resistance. Treatment of intestinal explants for 4 h with 10 µM DON induced morphological lesions and up-regulated the expression of pro-inflammatory cytokines as measured by qPCR and pan-genomic microarray analysis. By contrast, expression profile of D3G-treated explants was similar to that of controls, and these explants did not show histomorphology alteration. In conclusion, our data demonstrated that glucosylation of DON suppresses its ability to bind to the ribosome and decreases its intestinal toxicity.

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Section: Figsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

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Intestinal toxicity of the masked mycotoxin deoxynivalenol-3-β-d-glucoside

et al. 2015

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“…(20). Evidence that DON-3G is almost completely hydrolyzed in the digestive tract of rats, pigs, and humans has been presented (21)(22)(23).…”

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confidence: 99%

A Versatile Family 3 Glycoside Hydrolase from Bifidobacterium adolescentis Hydrolyzes β-Glucosides of the Fusarium Mycotoxins Deoxynivalenol, Nivalenol, and HT-2 Toxin in Cereal Matrices

Michlmayr

Varga

Malachová

et al. 2015

Appl Environ Microbiol

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Infestation of cereals by phytopathogenic fungi is a global threat to the human food supply. In addition to economically devastating losses through yield and quality deterioration of agricultural products, contamination with mycotoxins poses a serious challenge for food safety (1). Among the most relevant mycotoxin producers worldwide are Fusarium species, causing Fusarium head blight disease of small-grain cereals (FHB; also known as Fusarium ear blight or scab). Trichothecene class mycotoxins inhibit eukaryotic protein synthesis and are important Fusarium virulence factors. Furthermore, they can cause apoptotic cell death and immunosuppression and trigger proinflammatory responses in humans and animals (1-3). The most important groups with regard to food safety are type A (T-2 toxin and HT-2 toxin [HT2]) and type B (nivalenol [NIV] and deoxynivalenol [DON]) trichothecenes (4). The type A trichothecene T-2 toxin possesses high acute toxicity and has caused fatal outbreaks of alimentary toxic aleukia in the last century (1). DON is the predominant trichothecene toxin produced by the Fusarium graminearum species complex and ranks among the most frequent contaminants of cereals. Although the acute toxicity of DON is lower than that of type A trichothecenes, its ubiquitous presence in Fusarium-infected cereals creates an important food safety issue (2). Acute symptoms of DON ingestion are gastroenteritis and emesis (hence, the colloquial term vomitoxin). Maximum levels for DON in cereal-based foodstuff are set in Commission Regulation 1881/2006 (5), and indicative levels are provided for the sum of T-2 toxin and HT-2 toxin in Commission Recommendation 2013/165/EU (6) in Europe to protect consumers.The glycosylation of small molecules is a major route to inactivate endogenous and exogenous (xenobiotic) metabolites in plants (7-9). For example, formation of DON-3-O-␤-D-glucopyranoside (DON-3G) is an important factor in plant defense against FHB and has been proposed to be the molecular basis of the still-unidentified FHB1 gene (Fusarium head blight resistance quantitative trait locus) in wheat (10). DON-3G has been detected in a wide range of cereal commodities, with concentrations of about 20% relative to that of DON (11,12). However, high regional and seasonal variations have been reported, and in some cases, the content of DON-3G even exceeded that of DON (13,14). Evidence for glucosylated metabolites of NIV and type A trichothecenes has been presented as well (15)(16)(17). Such glucoconjugates of plant origin have been termed masked mycotoxins (13, 18), implying that they escape detection through

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“…The bioavailability of D3G is a subject of ongoing research . The latest studies on rats and pigs indicated that D3G partly contributes to the total DON intake (Nagl et al ., 2012;Nagl et al ., 2014) . Authors of another study dealing with the bioavailability of masked mycotoxins confirmed that DON conjugates were effectively deconjugated by the human colonic microbiota releasing parent DON (Dall'Erta et al ., 2013) .…”

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confidence: 99%

Analytical strategies for the determination of deoxynivalenol and its modified forms in beer: A mini review.

Malachová¹,

Varga²,

Schwartz-Zimmermann³

et al. 2015

Kvasny Prum

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Analytical strategies for the determination of deoxynivalenol and its modified forms in beer: A mini review. Kvasny Prum . 61, 2015, No . 2, pp . 46-50 The aim of this review is to provide a brief overview of analytical methods used for the determination of deoxynivalenol and its modified forms deoxynivalenol-3-β-D-glucoside, 3-acetyl-deoxynivalenol and 15-acetyl-deoxynivalenol in beer . The analytical methods discussed involve gas chromatography coupled with flame ionization detection, electron capture detection and mass spectrometry as well as liquid chromatography hyphenated to ultra-violet detection and mass spectrometry . Special attention was paid to sample preparation . Immunochemical methods such as enzyme-linked immunosorbent assays (ELISAs) which represent efficient tools for fast screening of beer with no sample purification are also discussed .

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Metabolism of the masked mycotoxin deoxynivalenol-3-glucoside in pigs

Cited by 142 publications

References 42 publications

Intestinal toxicity of the masked mycotoxin deoxynivalenol-3-β-d-glucoside

Intestinal toxicity of the masked mycotoxin deoxynivalenol-3-β-d-glucoside

A Versatile Family 3 Glycoside Hydrolase from Bifidobacterium adolescentis Hydrolyzes β-Glucosides of the Fusarium Mycotoxins Deoxynivalenol, Nivalenol, and HT-2 Toxin in Cereal Matrices

Analytical strategies for the determination of deoxynivalenol and its modified forms in beer: A mini review.

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