No abstract

Mycotoxins are important food contaminants that commonly co-occur with modified mycotoxins such as mycotoxin-glucosides in contaminated cereal grains. These masked mycotoxins are less toxic, but their breakdown and release of unconjugated mycotoxins has been shown by mixed gut microbiota of humans and animals. The role of different bacteria in hydrolysing mycotoxin-glucosides is unknown, and this study therefore investigated fourteen strains of human gut bacteria for their ability to break down masked mycotoxins. Individual bacterial strains were incubated anaerobically with masked mycotoxins (deoxynivalenol-3-β-glucoside, DON-Glc; nivalenol-3-β-glucoside, NIV-Glc; HT-2-β-glucoside, HT-2-Glc; diacetoxyscirpenol-α-glucoside, DAS-Glc), or unconjugated mycotoxins (DON, NIV, HT-2, T-2, and DAS) for up to 48 h. Bacterial growth, hydrolysis of mycotoxin-glucosides and further metabolism of mycotoxins were assessed. We found no impact of any mycotoxin on bacterial growth. We have demonstrated that Butyrivibrio fibrisolvens, Roseburia intestinalis and Eubacterium rectale hydrolyse DON-Glc, HT-2 Glc, and NIV-Glc efficiently and have confirmed this activity in Bifidobacterium adolescentis and Lactiplantibacillus plantarum (DON-Glc only). Prevotella copri and B. fibrisolvens efficiently de-acetylated T-2 and DAS, but none of the bacteria were capable of de-epoxydation or hydrolysis of α-glucosides. In summary we have identified key bacteria involved in hydrolysing mycotoxin-glucosides and de-acetylating type A trichothecenes in the human gut.

Small grain cereals are frequently infected with mycotoxigenic Fusarium fungi. Oats have a particularly high risk of contamination with type A trichothecene mycotoxins; their glucoside conjugates have also been reported. Agronomy practices, cereal variety and weather conditions have been suggested to play a role in Fusarium infection in oats. The current study investigates concentrations of free and conjugated Fusarium mycotoxins in organic and conventional oats grown in Scotland. In 2019, 33 milling oat samples (12 organic, 21 conventional) were collected from farmers across Scotland, together with sample questionnaires. Samples were analysed for 12 mycotoxins (type A trichothecenes T-2-toxin, HT-2-toxin, diacetoxyscirpenol; type B trichothecenes deoxynivalenol, nivalenol; zearalenone and their respective glucosides) using LC-MS/MS. The prevalence of type A trichothecenes T-2/HT-2 was very high (100% of conventional oats, 83% of organic oats), whereas type B trichothecenes were less prevalent, and zearalenone was rarely found. T-2-glucoside and deoxynivalenol-glucoside were the most prevalent conjugated mycotoxins (36 and 33%), and co-occurrence between type A and B trichothecenes were frequently observed (66% of samples). Organic oats were contaminated at significantly lower average concentrations than conventional oats, whereas the effect of weather parameters were not statistically significant. Our results clearly indicate that free and conjugated T-2- and HT-2-toxins pose a major risk to Scottish oat production and that organic production and crop rotation offer potential mitigation strategies.

No abstract

Mycotoxins are fungal secondary metabolites which are frequently detected in agricultural crops including cereals. They are potent toxins and are important food contaminants which pose a potential risk to consumer health. In addition to fungal mycotoxins, plantderived mycotoxin metabolites, also called masked mycotoxins, are frequently found in cereals. These masked mycotoxins are sugarbound metabolites, and their contribution to overall toxicity in humans is less well understood. Hence, this study used a range of in-vitro model systems to predict the intestinal fate of masked mycotoxins in the human gut. The mycotoxins studied included the prevalent Fusarium mycotoxins deoxynivalenol (DON), nivalenol (NIV), T2-toxin (T2), HT2-toxin (HT2) and diacetoxyscripenol (DAS) and their respective glucose-bound metabolites DON-Glc, NIV-Glc, T2-Glc, HT2-Glc, DAS-Glc.Artificial digestive juices (saliva, gastric juice, duodenal juice) were used to assess the stability of mycotoxins and masked mycotoxins in the small intestine. Human Caco-2 cells were used to study transport, metabolism and toxicity of mycotoxins (1) . Fully differentiated Caco-2 cultures were exposed to individual mycotoxins in culture medium in the apical compartment of Transwell filters and absorption and barrier disruption were assessed after 24 hours. Faecal batch cultures using human stool samples and single-strain incubations with important human gut strains were used to assess microbial metabolism of mycotoxins (2) . Individual mycotoxins were spiked into microbial cultures and incubated anaerobically for up to 48 hours. Mycotoxins were analysed using LC-MS/MS.None of the mycotoxins or masked mycotoxins were metabolised by small intestinal juices and absorption studies showed that free mycotoxins are readily absorbed and can disrupt intestinal barrier function. In contrast, masked mycotoxins are not absorbed though the epithelial monolayer intact and can hence be transported to the large intestine. Upon contact with microbiota, masked mycotoxins were readily hydrolysed and free mycotoxins released into the culture supernatant. Marked differences were observed in the hydrolysis rates between different donor samples as well as between different masked mycotoxins treated with the same donor sample. Microbial de-acetylation was observed for several mycotoxin in all donor samples, whereas de-epoxydation was rare.These results suggest that human gut microbiota are not efficient in detoxifying dietary mycotoxins. The rapid release of free mycotoxins from masked forms by human gut microbiota demonstrates that masked mycotoxins will contribute towards overall toxicity in humans and need to be included in risk assessments.