Deoxynivalenol and Zearalenone: Different Mycotoxins with Different Toxic Effects in the Sertoli Cells of Equus asinus

Abstract

(1) Background: Deoxynivalenol (DON) and zearalenone (ZEA) are type B trichothecene mycotoxins that exert serious toxic effects on the reproduction of domestic animals. However, there is little information about the toxicity of mycotoxins on testis development in Equus asinus. This study investigated the biological effects of DON and ZEA exposure on Sertoli cells (SCs) of Equus asinus; (2) Methods: We administered 10 μM and 30 μM DON and ZEA to cells cultured in vitro; (3) Results: The results showed that 10 μM DON exposure remarkably changed pyroptosis-associated genes and that 30 μM ZEA exposure changed inflammation-associated genes in SCs. The mRNA expression of cancer-promoting genes was remarkably upregulated in the cells exposed to DON or 30 μM ZEA; in particular, DON and ZEA remarkably disturbed the expression of androgen and oestrogen secretion-related genes. Furthermore, quantitative RT-PCR, Western blot, and immunofluorescence analyses verified the different expression patterns of related genes in DON- and ZEA-exposed SCs; (4) Conclusions: Collectively, these results illustrated the impact of exposure to different toxins and concrete toxicity on the mRNA expression of SCs from Equus asinus in vitro.

Pyroptosis-Mediated Damage Mechanism by Deoxynivalenol in Porcine Small Intestinal Epithelial Cells

“…Inflammasomes are multimolecular protein complexes consisting of apoptosis-associated speck-like proteins containing a caspase recruitment domain (ASC), nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs), and CASP1, and they act as an important factor in the inflammatory response to endogenous damage and exogenous pathogens, such as cytosolic double-stranded DNA, bacterial infection, crystals, and toxins [30]. Inflammasomes facilitate the activation of caspase 1 (CASP1), leading to the activation of Gasdermin D (GSDMD), thereby triggering cell membrane pore formation, which induces pyroptosis [31][32][33].…”

A high-throughput gut-on-chip platform to study the epithelial responses to enterotoxins

“…The sustained state of low-grade inflammation associated with chronic toxin exposure could therefore contribute to the development of these inflammatory diseases. Furthermore, co-occurrence of mycotoxins and bacterial toxins is now a matter of concern for food safety authorities, as this may lead to additive or synergic cytotoxic effects 17 , 18 . Thus, considering the severe pathological implications tied to enterotoxin exposure, precise evaluation of enterotoxin-specific epithelial toxicity is needed to establish safe enterotoxin exposure thresholds.…”