Deoxynivalenol (DON) and zearalenone (ZEN) are mycotoxins produced by fungi of the genus Fusarium which frequently contaminate maize and grain cereals. Mycotoxin-contaminated feed endangers animal health and leads to economic losses in animal production. Several mycotoxin elimination strategies, including the use of commercially available DON and ZEN detoxifying agents, have been developed. However, frequently there is no scientific proof of the efficacy of such adsorbents and degrading products. We therefore tested 20 commercially available products claiming to detoxify DON and/or ZEN either by biodegradation (4 products) or a combination of degradation and adsorption (16 products) under aerobic and anaerobic conditions at approx. pH 7. Under the applied conditions, a complete reduction of DON and consequent formation of the known non-toxic metabolite DOM-1 was exclusively observed in samples taken from the anaerobic degradation experiment of one product. For all other products, incubated under aerobic and anaerobic conditions, a maximum DON reduction of 17% after 72 h of incubation was detected. Aerobic and anaerobic incubation of only one tested product resulted in complete ZEN reduction as well as in the formation of the less-toxic metabolites DHZEN and HZEN. With this product, 68-97% of the toxin was metabolised within 3 h. After 24 h, a ZEN reduction ≥ 60% was obtained with four additional products during aerobic incubation only. Six of the 20 investigated products produced α- and/or β-ZEL, which are metabolites showing similar oestrogenic activity compared to ZEN. Aerobic and anaerobic degradation to unknown metabolites with unidentified toxicity was obtained with 10 and 3 products, respectively. The results of our study demonstrate the importance of in vitro experiments to critically screen agents claiming mycotoxin detoxification.
Fumonisins are among the most prevalent mycotoxins in feedstuffs. They disrupt the sphingolipid metabolism, thereby inducing a plethora of toxic effects in livestock. Supplementation with mycotoxin-degrading enzymes is a promising strategy for the detoxification of feedstuffs in the animals’ gastrointestinal tract. Here, we evaluated the suitability of the fumonisin esterase FumD as a feed additive (FUMzyme®) for the prevention of fumonisin toxicity in pigs by using a combination of different fumonisin biomarkers (sphinganine to sphingosine (Sa/So) ratio in serum and organs, concentrations of fumonisin B1 and hydrolysed derivatives in urine and faeces). In a pre-trial, we exposed pigs to 30 mg/kg fumonisins in feed and found the minimum effective dose of FUMzyme to be 15 U/kg. In a second trial we investigated the long-term efficacy of this minimum effective FUMzyme dose to counteract toxic effects elicited by 6 weeks of exposure to 2.5 mg/kg fumonisins in a diet containing naturally contaminated maize. Supplementation of feed with the minimum effective FUMzyme dose prevented an increase in the Sa/So ratio in serum and kidneys of fumonisin exposed pigs. The Sa/So ratio in serum proved to be the most reliable biomarker. The fumonisin pattern in faeces was less suitable as biomarker for assessing the efficacy of FUMzyme due to natural gastrointestinal hydrolysis of fumonisins. Analysis of urine samples provided additional information about gastrointestinal fumonisin hydrolysis before fumonisin absorption, but was analytically challenging because of low urinary fumonisin concentrations.
Food processing may induce thermal degradation of fumonisins in corn via Maillard-type reactions, or alkaline hydrolysis via loss of the two tricarballylic acid moieties. In the former case, N-(1-deoxy-D-fructos-1-yl)-fumonisin B(1) (NDF) can be formed, while the latter derivative is called hydrolysed fumonisin B(1) (HFB(1)). The aim of this study was to deepen the knowledge about the gastrointestinal stability of HFB(1) and NDF in humans. Due to the lack of standard, NDF was chemically synthesised and cleaned up in high purity to be used for further experiments. While NDF is already partially cleaved (about 41%) during simulated digestion, it remained rather stable towards human colon microflora. In contrast to this, HFB(1) is partially metabolised by the colon microflora to unknown compounds after 24 h of fermentation, as seen by a loss of about 22%. Concluding, the cleavage of NDF during digestion as well as the likely metabolisation of HFB(1) emphasise the need for animal trials to ascertain their toxicity in vivo.
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