The aim of this research was to evaluate the potential protective mechanism of astaxanthin (ASTA) against oxidative damage and inflammation caused by ochratoxin (OTA) in mouse lung. We divided mice into a control group (CG), an OTA group (PG), an astaxanthin group (AG), and an OTA+ASTA group (JG). Oxidative indices (malondialdehyde (MDA), total superoxide dismutase (T-SOD), and reduced glutathione (GSH)) and inflammatory markers (interleukin 1β (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α)) were assayed in the lung, and the lung-weight-to-body-weight ratio was calculated. Apoptosis was detected in pathological sections by the TdT-mediated dUTP nick-end labeling (TUNEL) assay. Oxidative damage and inflammation were detected in the lung of mice after exposure to OTA. Besides, Nrf2- and NF-κB-pathway-associated proteins were detected by Western blot. In contrast with OTA, ASTA significantly raised the expression of Nrf2, HO-1, and MnSOD, while the expression of other proteins (Keap1, TLR4, and NF-κB) was significantly decreased. These results indicate that ASTA exerted protective effects against OTA-induced oxidative damage and inflammation in the lung by regulating the Nrf2 and NF-κB pathways.

This study evaluated the protective effect of proanthocyanidins (PCs) on reducing apoptosis in the mouse intestinal epithelial cell model MODE-K exposed to zearalenone (ZEA) through inhibition of the endoplasmic reticulum stress (ERS)-induced apoptosis pathway. Our results showed that PCs could reduce the rate of apoptosis in MODE-K cells exposed to ZEA (p < 0.01). PCs significantly increased the ZEA-induced antioxidant protective effects on the enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and on the content of GSH. PCs also significantly decreased the ZEA-induced increase in the content of malondialdehyde (MDA). The analysis indicated that ZEA increased both mRNA and protein expression levels of C/EBP homologous protein (CHOP), GRP78, c-Jun N-terminal kinase (JNK), and cysteinyl aspartate specific proteinase 12 (caspase-12) (p < 0.05), which are related to the ERS-induced apoptosis pathway. ZEA decreased levels of the pro-apoptotic related protein Bcl-2 (p < 0.05) and increased the anti-apoptotic related protein Bax (p < 0.05). Co-treatment with PCs was also shown to significantly reverse the expression levels of these proteins in MODE-K cells. The results demonstrated that PCs could protect MODE-K cells from oxidative stress and apoptosis induced by ZEA. The underlying mechanism may be that PCs can alleviate apoptosis in mouse intestinal epithelial cells by inhibition of the ERS-induced apoptosis pathway.

Zearalenone (ZEN), an important environmental pollutant, can cause serious harm to human and animal health. The aim of our study was to examine the effect of zearalenone (ZEN) on miRNA expression profiles in the mouse Leydig cell line (TM3 Leydig cell line) by miRNA sequencing. The effect of ZEN on the viability of TM3 Leydig cells was verified by Cell Counting Kit-8 (CCK-8). MiRNA sequencing was performed 24 h after the exposure of TM3 Leydig cells with 50 μmol/L of ZEN. Bioinformatics predicted the miRNA target genes, performed Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, and conducted miRNA-gene-pathway mapping to show the relationship between miRNA, the target gene, and the signalling pathway. The expression levels of miRNA and the miRNA target genes associated with ZEN toxicology were verified by quantitative real-time polymerase chain reaction. The miRNA sequencing revealed a significant change (p < 0.05) in the 197 miRNAs in the ZEN-treated and control groups, among which 86 were up-regulated and 111 were down-regulated. GO analysis of the target genes of these miRNAs indicated various biological functions. KEGG analysis showed that the predicted miRNA target genes were involved in signalling pathways, such as cancer, apoptosis, and oxidation, namely, the Ras signalling pathway, Rap1 signalling pathway, PI3K-AKT signalling pathway, Foxo signalling pathway, and AMPK signalling pathway. These results suggest that ZEN, as an estrogen-like toxin, is regulated by microRNAs. Our results can help to examine the toxicological effects of ZEN-regulated miRNAs on germ cells.

Zearalenone (ZEA) contamination is a very serious problem around the world as it can induce reproductive disorders in animals and affect the health of humans. Therefore, reducing the damage it causes to humans and animals is a current focus of research. In this study, we assess the removing capacity of Pediococcus pentosaceus xy46 towards ZEA and investigate the mechanism responsible for its action, thus confirming if it can alleviate ZEA toxicity to the reproductive systems of male mice. Our results show that the rate at which the strain removes ZEA is as high as 89.2% in 48 h when the concentration of ZEA is 4 μg/mL in the liquid medium. Heat and acid treatment significantly enhanced the ability of the bacteria to remove ZEA. The animal experiments results show that the oral administration of xy46 to mice (0.2 mL daily at a concentration of 10⁹ CFU/mL for 28 days) significantly reduces the degree of testicular pathomorphological changes and apoptosis induced by ZEA when the mice are intragastric administration with 40 mg/kg ZEA daily for 28 days. Moreover, oral administration of xy46 enhances the decrease in the testosterone level and improves the oxidative stress injury induced by ZEA. Furthermore, oral administration of xy46 reverts the expression of these genes and proteins in the testicular tissues of the mice involved in the blood–testis barrier and apoptosis (e.g., Vim, caspase 12, Cldn11, N-cad, Bax, and Bcl-2). However, xy46 cannot significantly revert in some of these evaluated parameters, especially in sperm quantity and quality when the mice were given 70 mg/kg ZEA daily for 28 days. In conclusion, our results suggest that the strain Pediococcus pentosaceus xy46 can efficiently remove ZEA from the liquid medium, the mechanism responsible for its action is absorption, and it can alleviate the toxicity of ZEA to the reproductive systems of male mice when the mice are given 40 mg/kg ZEA daily, However, it cannot completely alleviate the reproductive toxicity of higher dosage of zearalenone through its ability to adsorb ZEA.