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- Deoxynivalenol (2)
- Acetyl-DON (1)
- Brassicaceae (1)
- Claviceps purpurea (1)
- Cyanobacterial toxin (1)
- Cylindrospermopsin (1)
- DON-3-glucoside (1)
- Deoxynivalenol (DON) (1)
- ERM (1)
- Ergotamine (1)
Toxin-producing cyanobacterial species are increasingly being found in freshwater systems. However, literature on the impact of many cyanobacterial toxins on plants is scarce. Cylindrospermosin (CYN), a secondary metabolite of cyanobacteria such as Cylindrospermopsis and Aphanizomenon species, is a potent hepatotoxin and protein synthesis inhibitor. Worryingly, CYN is increasingly found in surface and drinking water worldwide causing human and animal intoxications. Further, exposure of crop plants to CYN by irrigation with contaminated water has already been shown. Therefore, in this study, horticulturally important and highly consumed Brassica species were investigated to determine the level of CYN in the leaves after exposure of the roots to the toxin. Treatment of Brassica oleracea var. sabellica, Brassica juncea, and Sinapis alba under varying experimental conditions showed significant CYN uptake, with CYN levels ranging from 10% to 21% in the leaves compared to the CYN concentration applied to the roots (18–35 µg/l). In seedlings, CYN concentrations of up to 49 µg/g fresh weight were observed. Thus, crop plants irrigated with CYN-containing water may represent a significant source of this toxin within the food chain.
Germination induces the glucosylation of the Fusarium mycotoxin deoxynivalenol in various grains
(2012)
In food, the mycotoxin deoxynivalenol (DON) often occurs in conjunction with its 3-β-D-glucopyranoside (D3G). The transformation of DON to D3G through glucosylation is catalysed by plant enzymes, however, the exact circumstances are not well understood. In order to investigate the role of enzymatic glucosylation in germinating grains, DON treated kernels were steeped and germinated under laboratory conditions. Furthermore, the effect of malting on the DON content of the contaminated barley was investigated. In all cases, DON and its derivatives were quantified by HPLC-MS/MS before, during and after the experiments. Amongst the six tested cereals; wheat, rye, barley, spelt, and millet transformed DON to D3G during germination whilst the oats were inactive. For wheat, barley, and spelt the initial DON content was reduced by 50%, with the loss being almost entirely accounted for by D3G formation. As D3G might be cleaved during digestion, the elevated D3G concentration may obscure the toxicologically relevant DON content in processed food and beer. The germination process has a major influence on the 'masking' of DON, leading to high quantities of D3G that may be missed in common mycotoxin analyses.
Deoxynivalenol (DON) is one of the most abundant mycotoxins contaminating food and feed worldwide. Upon absorption, the major portion of the toxin is excreted by humans and animal species as glucuronide. However, consistent in vitro data on DON glucuronidation are lacking. In the present study, the metabolism of DON was investigated using liver microsomes from humans and six different animal species. It was shown that all animal and human liver microsomes led to the formation of up to three different mono-O-glucuronides with significant interspecies differences. While the activity of human liver microsomes was low (0.8 to 2.2 pmol·min–1·mg–1), bovine liver and rat liver microsomes conjugated DON with activities of 525 pmol·min–1·mg–1 and 80 pmol·min–1·mg–1, respectively.
The degradation and epimerization of ergot alkaloids (EAs) in rye flour were investigated after baking cookies and subsequently subjecting them to an in vitro digestion model. Different steps of digestion were analyzed using salivary, gastric, and duodenal juices. The degradation and bidirectional conversion of the toxicologically relevant (R)-epimers and the biologically inactive (S)-epimers for seven pairs of EAs were determined by a HPLC method coupled with fluorescence detection. Baking cookies resulted in degradation of EAs (2–30 %) and a shift in the epimeric ratio toward the (S)-epimer for all EAs. The applied digestion model led to a selective toxification of ergotamine and ergosine, two ergotamine-type EAs. The initial percentage of the toxic (R)-epimer in relation to the total toxin content was considerably increased after digestion of cookies. Ergotamine and ergosine increased from 32 to 51 % and 35 to 55 %, respectively. In contrast, EAs of the ergotoxine type (ergocornine, α- and β-ergocryptine, and ergocristine) showed an epimeric shift toward their biologically inactive (S)-epimers. Further experiments indicated that the selective epimerization of ergotamine EAs occurs in the duodenal juice only. These results demonstrate that toxification of EAs in the intestinal tract should be taken into consideration.