No abstract

Zearalenone (ZON) is a potent estrogenic mycotoxin produced by several Fusarium species most frequently on maize and therefore can be found in food and animal feed. Since animal production performance is negatively affected by the presence of ZON, its detoxification in contaminated plant material or by-products of bioethanol production would be advantageous. Microbial biotransformation into nontoxic metabolites is one promising approach. In this study the main transformation product of ZON formed by the yeast Trichosporon mycotoxinivorans was identified and characterized by liquid chromatography-tandem mass spectrometry (LC-MS/MS) and LC-diode array detector (DAD) analysis. The metabolite, named ZOM-1, was purified, and its molecular formula, Zearalenone (ZON) is the main member of a growing family of biologically important "resorcylic acid lactones" (RALs), which have been found in nature. ZON is produced by several Fusarium species, which colonize maize, barley, oat, wheat, and sorghum and tend to develop ZON during prolonged cool, wet growing and harvest seasons (38). Maize is the most frequently contaminated crop plant, and therefore, ZON can be found frequently in animal feeding stuff. Occurrence, toxicity, and metabolism data of ZON were summarized by the European Food Safety Authority (EFSA) (5) and in recent reviews (12,38).The potent xenohormone ZON leads to hyperestrogenism symptoms and in extreme cases to infertility problems, especially in pigs (15). Ovarian changes in pigs have been noted with toxin levels as low as of 50 g/kg in the diet (1). Ruminants are more tolerant to ZON ingestion; however, hyperestrogenic syndrome, including restlessness, diarrhea, infertility, decreased milk yields, and abortion, have been well documented with cattle and sheep (4, 29).Because widespread ZON contamination in feed can occur in problematic years, efficient ways to detoxify are desirable. The transformation of mycotoxins to nontoxic metabolites by pure cultures of microorganisms or by cell-free enzyme preparations (3) is an attractive possibility. Microbial metabolization of ZON to alpha-ZOL and beta-ZOL cannot be regarded as detoxification, because both ZOL products are still estrogenic (14). Also, formation of ZON-glucosides and -diglucosides (8, 17) and ZON-sulfate (7) cannot be considered true detoxification but rather formation of masked mycotoxins, because the conjugates may be hydrolyzed during digestion (11,23), releasing ZON again (2).As the estrogenic activity of ZON and its derivates can be explained by its chemical structure, which resembles natural estrogens (20), it can be expected that cleavage of the lactone undecyl ring system of ZON results in permanent detoxification.El-Sharkawy and Abul-Hajj (9) were the first to report inactivation of ZON after opening of the lactone ring by Gliocladium roseum. This filamentous fungus was capable of metabolizing ZON in yields of 80 to 90%. Also Takahashi-Ando et al. (31) described the degradation reaction of ZON with Clonostachys rosea (synonym of G. roseum...

No abstract

The contamination of animal feed with mycotoxins represents a worldwide problem for the animal industry. The most applied method for protecting animals against aflatoxicosis is the utilization of clay minerals. In the course of a research project adsorption experiments were performed in buffer solutions in order to evaluate the ability to bind Aflatoxin B1 (AfB1) at various pH-values. In order to investigate the strength of binding, the chemisorption index was calculated. Isothermal analysis was used to determine the values for the maximum adsorption capacity. Adsorption experiments in simulated gastrointestinal fluid and real gastric juice were carried out. Furthermore binding capability of the materials regarding selected vitamins was examined. Special attention was paid to the formation of AfB2a during experimental conditions. Based on the obtainedin vitro results, highly promising sorbent materials were ranked for furtherin vivo studies. Some adsorbing bentonites were also analysed mineralogically, but the results did not indicate which smectite property influences the adsorption process for AfB1.

Aflatoxins are a class of mycotoxins that impair poultry health and performance. Some clays have the ability to adsorb aflatoxins. In our study, mineralogical composition of the tested clays was confirmed by powder X-ray diffraction and simultaneous thermal analysis and their properties like pH, electrical conductivity, exchangeable cations, cation exchange capacity and clay content were determined. For their in vitro assessment regarding aflatoxin B1 (AFB1) adsorption, adsorption tests under ‘intensified conditions’ (low adsorbent and high toxin concentration) were carried out in buffers at various pH values and in real gastric juice followed by isothermal analysis in phosphate buffer. In vivo we used a completely randomised design with 4 replicate pens of 5 chicks assigned to each dietary treatment from hatch to 21 days. Dietary treatments included a negative and a positive control diet (2 mg/kg AFB1), and treatment groups receiving 2 mg/kg AFB1 and 0.5% of one of 8 adsorbents. Results of in vitro experiments ranked the adsorbents as ‘good’ (R, MB, B7, M32, M34, M5; 6 bentonites containing a cis-vacant smectite), ‘average’ (bentonite C2 containing a trans-vacant smectite) or ‘poor’ (zeolite Z08, containing clinoptilolite). The addition of AFB1 significantly reduced feed intake and/or body weight gain of the chicks compared to the negative control and to the treatment groups, except for C2 and Z08. Except Z08, all adsorbents numerically decreased the liver weight compared to the AFB1-fed group. Kidney weights were significantly increased by the addition of AFB1 compared to the control and most adsorbents, except C2 and Z08. Similarly, ‘good’ adsorbents significantly prevented the decrease in serum albumin and serum total protein. The ability of adsorbents to ameliorate AFB1 toxicity in poultry basically correlated with the in vitro findings meaning that ‘poor’ and ‘average’ adsorbents did not (Z08) or only partially (C2) protect against AFB1 in vivo.