Aflatoxins, produced mainly by filamentous fungi Aspergillus flavus and Aspergillus parasiticus, are one of the most carcinogenic compounds that have adverse health effects on both humans and animals consuming contaminated food and feed, respectively. Aflatoxin B1 (AFB1) and aflatoxin B2 (AFB2) as well as aflatoxin G1(AFG1) and aflatoxin G2 (AFG2) occur in the contaminated foods and feed. In the case of dairy ruminants, after the consumption of feed contaminated with aflatoxins, aflatoxin metabolites [aflatoxin M1 (AFM1) and aflatoxin M2 (AFM2)] may appear in milk. Because of the health risk and the official maximum limits of aflatoxins, there is a need for application of fast and accurate testing methods. At present, there are several analytical methods applied in practice for determination of aflatoxins. The aim of this review is to provide a guide that summarizes worldwide aflatoxin regulations and analytical methods for determination of aflatoxins in different food and feed matrices, that helps in the decision to choose the most appropriate method that meets the practical requirements of fast and sensitive control of their contamination. Analytical options are outlined from the simplest and fastest methods with the smallest instrument requirements, through separation methods, to the latest hyphenated techniques.

Fumonisin B1 (FB1) is a harmful mycotoxin produced by Fusarium species, which results in oxidative stress leading to cell death in plants. FB1 perturbs the metabolism of sphingolipids and causes growth and yield reduction. This study was conducted to assess the role of ethylene in the production and metabolism of reactive oxygen species in the leaves of wild type (WT) and ethylene receptor mutant Never ripe (Nr) tomato and to elucidate the FB1-induced phytotoxic effects on the photosynthetic activity and antioxidant mechanisms triggered by FB1 stress. FB1 exposure resulted in significant ethylene emission in a concentration-dependent manner in both genotypes. Moreover, FB1 significantly affected the photosynthetic parameters of PSII and PSI and activated photoprotective mechanisms, such as non-photochemical quenching in both genotypes, especially under 10 µM FB1 concentration. Further, the net photosynthetic rate and stomatal conductance were significantly reduced in both genotypes in a FB1 dose-dependent manner. Interestingly, lipid peroxidation and loss of cell viability were also more pronounced in WT as compared to Nr leaves indicating the role of ethylene in cell death induction in the leaves. Thus, FB1-induced oxidative stress affected the working efficiency of PSI and PSII in both tomato genotypes. However, ethylene-dependent antioxidant enzymatic defense mechanisms were activated by FB1 and showed significantly elevated levels of superoxide dismutase (18.6%), ascorbate peroxidase (129.1%), and glutathione S-transferase activities (66.62%) in Nr mutants as compared to WT tomato plants confirming the role of ethylene in the regulation of cell death and defense mechanisms under the mycotoxin exposure.

Urinary biomarkers of mycotoxin exposure were evaluated in the case of healthy people (n = 41) and coeliac patients (n = 19) by using a multi-biomarker LC-MS/MS immunoaffinity based method capable to analyse biomarkers of nine mycotoxins, i.e., fumonisin B1 (FB1), fumonisin B2 (FB2), deoxynivalenol (DON), zearalenone (ZEN), ochratoxin A (OTA), Aflatoxin B1 (AFB1), T-2 toxin, HT-2 toxin and Nivalenol (NIV). Urinary biomarker concentrations were used to calculate the probable daily intake (PDI) of fumonisin B1, deoxynivalenol, zearalenone and ochratoxin A and compared with their tolerable daily intake (TDI). The human urinary excretion rate values reported in the literature and the 24 h excretion rate measured in piglets were used to estimate and compare the PDI values of the four mycotoxins. The highest mean biomarker concentrations were found for DON (2.30 ng/mL for healthy people and 2.68 ng/mL for coeliac patients). Mean OTA concentration was significantly higher (p < 0.001) in healthy people compared to coeliac patients. PDI calculated with piglets excretion data exceeded the TDI values by a much smaller percentage than when they were calculated from human data, especially for FB1. The uncertainties arising from the different calculations can be well perceived on the basis of these data.

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Fumonisins are frequent food contaminants. The high exposure to fumonisins can cause harmful effects in humans and animals. Fumonisin B1 (FB1) is the most typical member of this group; however, the occurrence of several other derivatives has been reported. Acylated metabolites of FB1 have also been described as possible food contaminants, and the very limited data available suggest their significantly higher toxicity compared to FB1. Furthermore, the physicochemical and toxicokinetic properties (e.g., albumin binding) of acyl-FB1 derivatives may show large differences compared to the parent mycotoxin. Therefore, we tested the interactions of FB1, N-palmitoyl-FB1 (N-pal-FB1), 5-O-palmitoyl-FB1 (5-O-pal-FB1), and fumonisin B4 (FB4) with human serum albumin as well as the toxic effects of these mycotoxins on zebrafish embryos were examined. Based on our results, the most important observations and conclusions are the following: (1) FB1 and FB4 bind to albumin with low affinity, while palmitoyl-FB1 derivatives form highly stable complexes with the protein. (2) N-pal-FB1 and 5-O-pal-FB1 likely occupy more high-affinity binding sites on albumin. (3) Among the mycotoxins tested, N-pal-FB1 showed the most toxic effects on zebrafish, followed by 5-O-pal-FB1, FB4, and FB1. (4) Our study provides the first in vivo toxicity data regarding N-pal-FB1, 5-O-pal-FB1, and FB4.