Zearalenone (ZEA) is an estrogenic and ochratoxin A (OTA) is a hepatotoxic Fusarium mycotoxin commonly seen in cereals and fruits products. No previous investigation has studied on a single platform for the multi degradation mycotoxin. The current study aimed to investigate the bifunctional activity of a novel fusion recombinant. We have generated a recombinant fusion enzyme (ZHDCP) by combining two single genes named zearalenone hydrolase (ZHD) and carboxypeptidase (CP) in frame deletion by crossover polymerase chain reaction (PCR). We identified enzymatic properties and cell cytotoxicity assay of ZHDCP enzyme. Our findings have demonstrated that ZEA was completely degraded to the non-toxic product in 2 h by ZHDCP enzyme at an optimum pH of 7 and a temperature of 35 °C. For the first time, it was found out that ZEA 60% was degraded by CP degrades in 48 h. Fusion ZHDCP and CP enzyme were able to degrade 100% OTA in 30 min at pH 7 and temperature 30 °C. ZEA- and OTA-induced cell death and increased cell apoptosis rate and regulated mRNA expression of Sirt1, Bax, Bcl2, Caspase3, TNFα, and IL6 genes. Our novel findings demonstrated that the fusion enzyme ZHDCP possess bifunctional activity (degrade OTA and ZEA), and it could be used to degrade more mycotoxins.

Mycotoxins are secondary metabolites of filamentous fungi that contaminate food products such as fruits, vegetables, cereals, beverages, and other agricultural commodities. Their occurrence in the food chain, especially in beverages, can pose a serious risk to human health, due to their toxicity, even at low concentrations. Mycotoxins, such as aflatoxins (AFs), ochratoxin A (OTA), patulin (PAT), fumonisins (FBs), trichothecenes (TCs), zearalenone (ZEN), and the alternaria toxins including alternariol, altenuene, and alternariol methyl ether have largely been identified in fruits and their derived products, such as beverages and drinks. The presence of mycotoxins in beverages is of high concern in some cases due to their levels being higher than the limits set by regulations. This review aims to summarize the toxicity of the major mycotoxins that occur in beverages, the methods available for their detection and quantification, and the strategies for their control. In addition, some novel techniques for controlling mycotoxins in the postharvest stage are highlighted.

Aflatoxins (AFs), deoxynivalenols (DONs), and zearalenones (ZENs) are common mycotoxins that contaminate feedstuff, causing contamination of poultry products. In our study, these mycotoxins were quantified in 152 egg samples collected from markets in Jiangsu (JS), Zhejiang (ZJ), and Shanghai (SH) and in 70 chicken tissue samples (liver, heart, and gizzard) from ZJ in China. The main mycotoxins observed in egg samples were DON, 15-AcDON, and ZEN, although only ZEN family mycotoxins (ZEN, α-ZEL, β-ZEL, and α-ZAL) were detected in chicken tissues. Furthermore, for the first time, we assessed the health risks of exposure of three populations (children, adults, and elder adults) to DONs (DON, 3-AcDON, and 15-AcDON) and ZEN in eggs (from three different areas) and to ZEN in chicken tissues. We show that the mean dietary intake (DI) values and the 97.5th percentile DI values of DON and ZEN through egg ingestion were lower than the provisional maximum tolerable daily intake (PMTDI) (1 μg/kg body weight (BW)/day) for the three populations in the three geographical areas studied. However, eggs contaminated with high levels of DONs and ZEN contributed to a large proportion of the PMTDI of these mycotoxins, especially in children and elder adults. Although ZEN was highly detected in the chicken tissues, no significant health risk was observed.

Fumonisin contaminates food and feed extensively throughout the world, causing chronic and acute toxicity in human and animals. Currently, studies on the toxicology of fumonisins mainly focus on fumonisin B1 (FB1). Considering that FB1, fumonisin B2 (FB2) and fumonisin B3 (FB3) could coexist in food and feed, a study regarding a single toxin, FB1, may not completely reflect the toxicity of fumonisin. The gastrointestinal tract is usually exposed to these dietary toxins. In our study, the human gastric epithelial cell line (GES-1) was used as in vitro model to evaluate the toxicity of fumonisin. Firstly, we found that they could cause a decrease in cell viability, and increase in membrane leakage, cell death and the induction of expression of markers for endoplasmic reticulum (ER) stress. Their toxicity potency rank is FB1 > FB2 >> FB3. The results also showed that the synergistic effect appeared in the combinations of FB1 + FB2 and FB1 + FB3. Nevertheless, the combinations of FB2 + FB3 and FB1 + FB2 + FB3 showed a synergistic effect at low concentration and an antagonistic effect at high concentration. We also found that myriocin (ISP-1) could alleviate the cytotoxicity induced by fumonisin in GES-1 cells. Finally, this study may help to determine or optimize the legal limits and risk assessment method of mycotoxins in food and feed and provide a potential method to block the fumonisin toxicity.

Ochratoxin A(OTA) is considered to be one of the most important contaminants of food and feed worldwide. The liver is one of key target organs for OTA to exert its toxic effects. Due to current lifestyle and diet, nonalcoholic fatty liver disease (NAFLD) has been the most common liver disease. To examine the potential effect of OTA on hepatic lipid metabolism and NAFLD, C57BL/6 male mice received 1 mg/kg OTA by gavage daily. Compared with controls, OTA increased lipid deposition and TG accumulation in mouse livers. In vitro OTA treatment also promoted lipid droplets accumulation in primary hepatocytes and HepG2 cells. Mechanistically, OTA prevented PPARγ degradation by reducing the interaction between PPARγ and its E3 ligase SIAH2, which led to activation of PPARγ signaling pathway. Furthermore, downregulation or inhibition of CD36, a known of PPARγ, alleviated OTA-induced lipid droplets deposition and TG accumulation. Therefore, OTA induces hepatic steatosis via PPARγ-CD36 axis, suggesting that OTA has an impact on liver lipid metabolism and may contribute to the development of metabolic diseases.