Deoxynivalenol (DON) is a mycotoxin mainly produced by the Fusarium graminearum complex, which are important phytopathogens that can infect crops and lead to a serious disease called Fusarium head blight (FHB). As the most common B type trichothecene mycotoxin, DON has toxic effects on animals and humans, which poses a risk to food security. Thus, efforts have been devoted to control DON contamination in different ways. Management of DON production by Trichoderma strains as a biological control-based strategy has drawn great attention recently. In our study, eight selected Trichoderma strains were evaluated for their antagonistic activities on F. graminearum by dual culture on potato dextrose agar (PDA) medium. As potential antagonists, Trichoderma strains showed prominent inhibitory effects on mycelial growth and mycotoxin production of F. graminearum. In addition, the modified mycotoxin deoxynivalenol-3-glucoside (D3G), which was once regarded as a detoxification product of DON in plant defense, was detected when Trichoderma were confronted with F. graminearum. The occurrence of D3G in F. graminearum and Trichoderma interaction was reported for the first time, and these findings provide evidence that Trichoderma strains possess a self-protection mechanism as plants to detoxify DON into D3G when competing with F. graminearum.

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.

Mycotoxin contamination is a significant health concern for human beings, but health risk assessments are usually based on one single mycotoxin, which might neglect the additive or competitive interactions between co‐occurring mycotoxins

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.

Fumonisins are mainly produced by Fusarium verticillioides and proliferatum, which causes a variety of toxicities in humans and animals, including fumonisin Bs (FBs) as the main form. After they are metabolized by plants or microorganisms, modified fumonisins are difficult to detect by conventional methods, which result in an underestimation of their contamination level. Fumonisins widely contaminate maize and maize products, especially in broiler feed. As an economically important food, broilers are often adversely affected by mycotoxins, leading to food safety hazards and high economic losses. However, there are few studies regarding the adverse effects of FBs on broiler growth and health, especially modified FBs. Our data shows that after exposure to FBs or hydrolyzed fumonisin Bs (HFBs), the body weight and tissue weight of broilers decreased significantly, especially the testes. Moreover, they significantly affect the intestinal microbiota and the relative abundance of bacteria from phylum-to-species levels, with the differentially affected bacteria mainly belonging to Firmicutes and Proteobacteria. Our findings suggest that both the parent and hydrolyzed FBs could induce growth retardation, tissue damage and the imbalance of intestinal microbiota in broilers. This indicated that the harmful effects of HFBs cannot be ignored during food safety risk assessment.