Suchergebnisse

Thirty-seven red yeast rice (RYR) food supplements were screened for their mycotoxin and natural statin content. Products included pure RYR capsules and multi-ingredient formulations with standardized amounts of monacolin K (MK), marketed both online and retail in the European Union. In terms of mycotoxins, citrinin (CIT) was found in all the monitored products. As CIT content ranged from 100 to 25100 μg/kg, only four products were compliant with maximum EU levels in force until April 2020, while a single product was compliant with the limit of 100 μg/kg introduced after that date. Four contaminated products were labeled as "citrinin free". In terms of natural statins, nine products had a lower content vs. label statements (from −30 to −83%), while for 24 a larger MK amount (from 10 to 266%) was noticed. Three products had a negligible MK content and only 19 offered a daily dosage exceeding 10 mg as dictated by the health claim granted by EFSA in the EU. No sample had label values compliant with pharmaceutical Good Manufacturing Practices requirements (95–105% content of active constituent). Variable, but small amounts of simvastatin (0.1–7.5 μg per daily dose) were found in 30 samples. These results suggest that limited efficacy and reported safety issues may stem from an under-regulated and undercontrolled market, weakening both effectiveness and risk assessment evaluations.

Insects are considered a suitable alternative feed for livestock production and their use is nowadays regulated in the European Union by the European Commission Regulation No. 893/2017. Insects have the ability to grow on a different spectrum of substrates, which could be naturally contaminated by mycotoxins. In the present work, the mycotoxin uptake and/or excretion in two different insect species, Alphitobius diaperinus (Lesser Mealworm, LM) and Hermetia illucens (Black Soldier Fly, BSF), grown on naturally contaminated substrates, was evaluated. Among all the substrates of growth tested, the Fusarium toxins deoxynivalenol (DON), fumonisin 1 and 2 (FB1 and FB2) and zearalenone (ZEN) were found in those based on wheat and/or corn. No mycotoxins were detected in BSF larvae, while quantifiable amount of DON and FB1 were found in LM larvae, although in lower concentration than those detected in the growing substrates and in the residual fractions. Mass balance calculations indicated that BSF and LM metabolized mycotoxins in forms not yet known, accumulating them in their body or excreting in the faeces. Further studies are required in this direction due to the future employment of insects as feedstuff.

International audience ; Fusarium mycotoxins are a relevant problem in the cereal supply chain at a worldwide level, being wheat, maize and barley the main contaminated crops; mould growth could happen in the pre-harvest phase and also during transport and storage due to ineffective drying conditions. Among Fusarium toxins, deoxynivalenol (DON) is considered the most important contaminant in wheat, due to its wide-spread occurrence. In the last years the European Food Safety Authority and the European Commission had frequently expressed opinions on Fusarium toxins, setting limits, regulations and guidelines in order to reduce their levels in raw materials and food commodities: in particular European legislation (Reg. 1881\2006) sets the maximum limit for deoxynivalenol in flour and bread as 750 µg/Kg and 500 µg/Kg respectively. Relatively few studies have taken into account the loss of trichothecenes during processing, focusing on how processing factors may influence their degradation. In particular, the description of DON behavior during bread-making is very difficult, since complex physic-chemical modifications occur during the transformation of raw ingredients into the final product. In the present study, we studied how DON concentration may be influenced by modifying bread-making parameters, with a special emphasis on the fermentation and baking stages, starting from a naturally contaminated flour at both pilot and industrial scales. Exploiting the power of a Design of Experiments (DoE) approach to consider the high complexity of the studied system, the obtained model shows satisfying goodness of fit and prediction, suggesting that the baking step (time/temperature ranges) is crucial for minimizing native DON level in bread.

The aim of this review is to give a comprehensive overview of the current knowledge on plant metabolites of mycotoxins, also called masked mycotoxins. Mycotoxins are secondary fungal metabolites, toxic to human and animals. Toxigenic fungi often grow on edible plants, thus contaminating food and feed. Plants, as living organisms, can alter the chemical structure of mycotoxins as part of their defence against xenobiotics. The extractable conjugated or non-extractable bound mycotoxins formed remain present in the plant tissue but are currently neither routinely screened for in food nor regulated by legislation, thus they may be considered masked. Fusarium mycotoxins (deoxynivalenol, zearalenone, fumonisins, nivalenol, fusarenon-X, T-2 toxin, HT-2 toxin, fusaric acid) are prone to metabolisation or binding by plants, but transformation of other mycotoxins by plants (ochratoxin A, patulin, destruxins) has also been described. Toxicological data are scarce, but several studies highlight the potential threat to consumer safety from these substances. In particular, the possible hydrolysis of masked mycotoxins back to their toxic parents during mammalian digestion raises concerns. Dedicated chapters of this article address plant metabolism as well as the occurrence of masked mycotoxins in food, analytical aspects for their determination, toxicology and their impact on stakeholders.

The aim of this review is to give a comprehensive overview of the current knowledge on plant metabolites of mycotoxins, also called masked mycotoxins. Mycotoxins are secondary fungal metabolites, toxic to human and animals. Toxigenic fungi often grow on edible plants, thus contaminating food and feed. Plants, as living organisms, can alter the chemical structure of mycotoxins as part of their defence against xenobiotics. The extractable conjugated or non-extractable bound mycotoxins formed remain present in the plant tissue but are currently neither routinely screened for in food nor regulated by legislation, thus they may be considered masked. Fusarium mycotoxins (deoxynivalenol, zearalenone, fumonisins, nivalenol, fusarenon-X, T-2 toxin, HT-2 toxin, fusaric acid) are prone to metabolisation or binding by plants, but transformation of other mycotoxins by plants (ochratoxin A, patulin, destruxins) has also been described. Toxicological data are scarce, but several studies highlight the potential threat to consumer safety from these substances. In particular, the possible hydrolysis of masked mycotoxins back to their toxic parents during mammalian digestion raises concerns. Dedicated chapters of this article address plant metabolism as well as the occurrence of masked mycotoxins in food, analytical aspects for their determination, toxicology and their impact on stakeholders.

The aim of this review is to give a comprehensive overview of the current knowledge on plant metabolites of mycotoxins, also called masked mycotoxins. Mycotoxins are secondary fungal metabolites, toxic to human and animals. Toxigenic fungi often grow on edible plants, thus contaminating food and feed. Plants, as living organisms, can alter the chemical structure of mycotoxins as part of their defence against xenobiotics. The extractable conjugated or non-extractable bound mycotoxins formed remain present in the plant tissue but are currently neither routinely screened for in food nor regulated by legislation, thus they may be considered masked. Fusarium mycotoxins (deoxynivalenol, zearalenone, fumonisins, nivalenol, fusarenon-X, T-2 toxin, HT-2 toxin, fusaric acid) are prone to metabolisation or binding by plants, but transformation of other mycotoxins by plants (ochratoxin A, patulin, destruxins) has also been described. Toxicological data are scarce, but several studies highlight the potential threat to consumer safety from these substances. In particular, the possible hydrolysis of masked mycotoxins back to their toxic parents during mammalian digestion raises concerns. Dedicated chapters of this article address plant metabolism as well as the occurrence of masked mycotoxins in food, analytical aspects for their determination, toxicology and their impact on stakeholders. ; peerReviewed

The aim of this review is to give a comprehensive overview of the current knowledge on plant metabolites of mycotoxins, also called masked mycotoxins. Mycotoxins are secondary fungal metabolites, toxic to human and animals. Toxigenic fungi often grow on edible plants, thus contaminating food and feed. Plants, as living organisms, can alter the chemical structure of mycotoxins as part of their defence against xenobiotics. The extractable conjugated or non-extractable bound mycotoxins formed remain present in the plant tissue but are currently neither routinely screened for in food nor regulated by legislation, thus they may be considered masked. Fusarium mycotoxins (deoxynivalenol, zearalenone, fumonisins, nivalenol, fusarenon-X, T-2 toxin, HT-2 toxin, fusaric acid) are prone to metabolisation or binding by plants, but transformation of other mycotoxins by plants (ochratoxin A, patulin, destruxins) has also been described. Toxicological data are scarce, but several studies highlight the potential threat to consumer safety from these substances. In particular, the possible hydrolysis of masked mycotoxins back to their toxic parents during mammalian digestion raises concerns. Dedicated chapters of this article address plant metabolism as well as the occurrence of masked mycotoxins in food, analytical aspects for their determination, toxicology and their impact on stakeholders.

The aim of this review is to give a comprehensive overview of the current knowledge on plant metabolites of mycotoxins, also called masked mycotoxins. Mycotoxins are secondary fungal metabolites, toxic to human and animals. Toxigenic fungi often grow on edible plants, thus contaminating food and feed. Plants, as living organisms, can alter the chemical structure of mycotoxins as part of their defence against xenobiotics. The extractable conjugated or non-extractable bound mycotoxins formed remain present in the plant tissue but are currently neither routinely screened for in food nor regulated by legislation, thus they may be considered masked. Fusarium mycotoxins (deoxynivalenol, zearalenone, fumonisins, nivalenol, fusarenon-X, T-2 toxin, HT-2 toxin, fusaric acid) are prone to metabolisation or binding by plants, but transformation of other mycotoxins by plants (ochratoxin A, patulin, destruxins) has also been described. Toxicological data are scarce, but several studies highlight the potential threat to consumer safety from these substances. In particular, the possible hydrolysis of masked mycotoxins back to their toxic parents during mammalian digestion raises concerns. Dedicated chapters of this article address plant metabolism as well as the occurrence of masked mycotoxins in food, analytical aspects for their determination, toxicology and their impact on stakeholders.

Maize is the principal staple food/feed crop exposed to mycotoxins, and the co-occurrence of multiple mycotoxins and their metabolites has been well docu- mented. This review presents the infection cycle, ecology, and plant-pathogen interac- tions of Aspergillus and Fusarium species in maize, and current knowledge on maize chain management to mitigate the occurrence of aflatoxins and fumonisins. Preven- tive actions include at pre-harvest, as part of cropping systems, at harvest, and at post- harvest, through storage, processing, and detoxification to minimize consumer expo- sure. Preventive actions in the field have been recognized as efficient for reducing the entrance of mycotoxins into production chains. Biological control of Aspergillus flavus has been recognized to minimize contamination with aflatoxins. Post-harvest maize grain management is also crucial to complete preventive actions, and has been made mandatory in government food and feed legislation.

Abstract
The present report describes the work performed in the EFSA‐project 'Data collection, update and further development of biologically‐based models for humans and animal species to support transparency in food and feed safety'. Here, Focus is given to case studies for food and feed chemicals to predict kinetic parameters and profiles using generic and substance‐specific physiologically‐based kinetic (PBK) models for humans, including human subgroups, laboratory animal species, farm animals and a kinetic‐dynamic model in salmon. For humans, five case studies were conducted to compare kinetic predictions using the human generic PBK 6‐compartment COSMOS/TKPlatewith i) in vivo data from human clinical or biomonitoring studies, ii) substance‐specific model predictions using molecules relevant to food safety. Another five case studies assessed the impact of physiological variability (including pregnancy, renal excretion, metabolism variability, or ontogeny) and their impact on biomarkers of exposure. Case studies on laboratory and farm animals focused on theophylline, caffeine, cannabinoids, alkaloids and mycotoxins using the generic 11/12 PBK compartment models integrated in EFSA's TKPlate to assess predicted and experimental parameters i.e. plasma concentrations, excretion via milk or eggs. Overall, predictions from the human generic and substance‐specific PBK models for parameters of chronic exposure were similar and robust compared to the available experimental data. For test species and farm animals, model predictions from the generic TKPlate PBK models also performed well and were mostly within 2‐fold compared to available experimental in vivo data. In addition, 3D molecular modelling case studies were also conducted to investigate transport of chemicals (ochratoxin A, perfluoroalkyls) and cytochrome P450 metabolism (ochratoxin A, safrole and other alkenylbenzenes) as a useful tool to generate metabolism information at the molecular level. Conclusions and recommendations for future work are formulated to further develop generic PBK models for parent compounds and metabolites and further guidance to use and parameterise these models in next generation risk assessment.