Carbon Quantum Dots Encapsulated Molecularly Imprinted Fluorescence Quenching Particles for Sensitive Detection of Zearalenone in Corn Sample.

An eco-friendly and efficient one-step approach for the synthesis of carbon quantum dots (CDs) that encapsulated molecularly imprinted fluorescence quenching particles (MIFQP) and their application for the determination of zearalenone (ZEA) in a cereal sample are described in this study. CDs with high luminescence were first synthesized, and then encapsulated in the silica-based matrix through a non-hydrolytic sol-gel process. The resulting ZEA-imprinted particles exhibited not only an excellent specific molecular recognition of ZEA, but also good photostability and obvious template binding-induced fluorescence quenching. Under the optimized conditions, the fluorescence intensity of MIFQP was inversely proportional to the concentration of ZEA. By validation, the detection range of these fluorescence quenching materials for ZEA was between 0.02 and 1.0 mg L-1, and the detection limit was 0.02 mg L-1 (S/N = 3). Finally, the MIFQP sensor was successfully applied for ZEA determination in corn with recoveries from 78% to 105% and the relative standard deviation (RSD %) was lower than 20%, which suggests its potential in actual applications.

Mycotoxins in commercial dry pet food in China.

The aim of this study was to investigate the occurrence of the most common mycotoxins in commercial dry dog food using liquid chromatography-tandem mass spectrometry (LC-MS/MS). Aflatoxin B1 (AFB1), aflatoxin G1 (AFG1), zearalenone (ZEN), deoxynivalenol (DON), T-2, beauvericin (BEA), citrinin (CIT), ochratoxin A (OTA), fumonisin B1 (FB1) were included in this study. The results showed that all these analytes could be found in the samples. Furthermore, only one sample was found free of mycotoxins contamination. All other samples (96.9%) were contaminated by at least three different types of mycotoxins. Among these mycotoxins, DON, ZEN, AFB1, FB1, CIT and BEA exhibited relatively high incidence, with occurrence rates of 78.1%, 62.5%, 87.5%, 93.8%, 68.8 and 96.9%, respectively. Furthermore, it is worth noting that AFB1 concentration in all AFB1 positive samples exceeded the maximum limits set by the European Union, with concentrations ranging from 30.3-242.7 µg/kg.

Zearalenone (ZEA)-induced intestinal inflammation is mediated by the NLRP3 inflammasome.

To ascertain whether zearalenone (ZEA) could induce intestinal inflammation and investigate its possible mechanism, we investigated inflammatory cytokine release and the activation of the NLRP3 inflammasome after ZEA treatment both in vitro or in vivo. First, intestinal porcine enterocyte cell line (IPEC-J2) cells and mouse peritoneal macrophages were treated with ZEA to detect NLRP3 inflammasome activation, and the role of reactive oxygen species (ROS) in ZEA-induced inflammation was investigated. Then, Balb/c mice were fed a gavage of ZEA, and the disease activity indices (DAIs) and histological analysis were used to assess intestinal inflammation. Our study showed that the mRNA expression of NLRP3 inflammasome, pro-interleukin-1ß (pro-IL-1ß), and pro-interleukin-18 (pro-IL-18) was up-regulated 0.5- to 1-fold and that the release of IL-1ß and IL-18 increased from 48 pg mL-1 to 55 pg mL-1 and 110 pg mL-1 to 145 pg mL-1, respectively. However, ROS inhibitor N-acetyl-l-cysteine (NAC) reduced IL-1ß and IL-18 release to 45 pg mL-1 and 108 pg mL-1. Moreover, the same phenomenon was observed in intestinal tissues of ZEA-treated mice. In addition, clinical parameters of treated mice showed stools became loose and contained mucous. In addition, the presence of gross blood stool was found in the last 2 d. Histological analysis showed obvious inflammatory cell infiltration and tissue damage in the colon. These findings uncovered a possible mechanism of intestinal mucosal innate immunity in response to mycotoxin ZEA that ZEA could activate the ROS-mediated NLRP3 inflammasome and, in turn, contribute to the caspase-1-dependent activation of the inflammatory cytokines IL-1ß and IL-18.