Fusarium-derived mycotoxin deoxynivalenol (DON) usually induces diarrhea, vomiting and gastrointestinal inflammation. We studied the cytotoxic effect of DON on porcine small intestinal epithelium using the intestinal porcine epithelial cell line IPEC-J2. We screened out differentially expressed genes (DEGs) using RNA-seq and identified 320 upregulated genes and 160 downregulated genes. The enrichment pathways of these DEGs focused on immune-related pathways. DON induced proinflammatory gene expression, including cytokines, chemokines and other inflammation-related genes. DON increased IL1A, IL6 and TNF-α release and DON activated the phosphorylation of extracellular signal-regulated kinase-1 and-2 (ERK1/2), JUN N-terminal kinase (JNK) and p38 MAPK. A p38 inhibitor attenuated DON-induced IL6, TNF-α, CXCL2, CXCL8, IL12A, IL1A, CCL20, CCL4 and IL15 production, while an ERK1/2 inhibitor had only a small inhibitory effect on IL15 and IL6. An inhibitor of p38 MAPK decreased the release of IL1A, IL6 and TNF-α and an inhibitor of ERK1/2 partly attenuated protein levels of IL6. These data demonstrate that DON induces proinflammatory factor production in IPEC-J2 cells by activating p38 and ERK1/2.

Deoxynivalenol (DON) is one of the most common contaminants of various foodstuffs. A biotransformation system was used in order to lessen the toxicity of DON. A strain of Aspergillus (NJA-1) was isolated from soil and cultured in an inorganic salt medium containing DON. Bt2a/Bt2b primers were used to amplify the β-tubulin gene of NJA-1. Sequence analysis the PCR product and morphology observation indicated that NJA-1 belonged to Aspergillus tubingensis (aerobic fungi). The DNA sequence information of the PCR product was deposited in GenBank (accession number DQ9025790). The DNA sequence had 99% similarity to the Aspergillus tubingensis accession number AY820009. An unknown compound in NJA-1 showed the ability to convert DON into another product. The molecular weight of the bioconversion product was 18.1 D (H₂O) larger than that of DON. The analysis showed that DON could be hydrolyzed by NJA-1. The mean DON biotransformation rate was 94.4% after two weeks of cultivation. The finding presents a new method for DON biotransformation.

Trichothecene mycotoxins are common contaminants in cereal grains and negatively impact human and animal health. Although anorexia is a common hallmark of type B trichothecenes-induced toxicity, less is known about the anorectic potencies of type A trichothecenes. The purpose of this study was to compare the anorectic potencies of four type A trichothecenes (T-2 toxin (T-2), HT-2 toxin (HT-2), diacetoxyscirpenol (DAS), and neosolaniol (NEO)) in mice. Following oral exposure to T-2, HT-2, DAS, and NEO, the no observed adverse effect levels (NOAELs) and lowest observed adverse effect levels (LOAELs) were 0.01, 0.01, 0.1, and 0.01 mg/kg body weight (BW), and 0.1, 0.1, 0.5, and 0.1 mg/kg BW, respectively. Following intraperitoneal (IP) exposure to T-2, HT-2, DAS, and NEO, the NOAELs were 0.01 mg/kg BW, except for DAS (less than 0.01 mg/kg BW), and the LOAELs were 0.1, 0.1, 0.01, and 0.1 mg/kg BW, respectively. Taken together, the results suggest that (1) type A trichothecenes could dose-dependently elicit anorectic responses following both oral gavage and IP exposure in mice; (2) the anorectic responses follow an approximate rank order of T-2 = HT-2 = NEO > DAS for oral exposure, and DAS > T-2 = HT-2 = NEO for IP administration; (3) IP exposure to T-2, HT-2, DAS, and NEO evoked stronger anorectic effects than oral exposure. From a public health perspective, comparative anorectic potency data should be useful for establishing toxic equivalency factors for type A trichothecenes.

Aflatoxin B₁ (AFB₁) and deoxynivalenol (DON) are important food-borne mycotoxins that have been implicated in animal and human health. In this study, individual and combinative effects of AFB₁ and DON were tested in primary hepatocytes of Cyprinus carpio. The results indicated that the combinative effects of AFB₁ and DON (0.01 μg/mL AFB₁ and 0.25 μg/mL DON; 0.02 μg/mL AFB₁ and 0.25 μg/mL DON; 0.02 μg/mL AFB₁ and 0.5 μg/mL DON) were higher than that of individual mycotoxin (P