Alleviation of Mycotoxin-Induced Toxicity

A special issue of Toxins (ISSN 2072-6651). This special issue belongs to the section "Mycotoxins".

Deadline for manuscript submissions: 28 February 2026 | Viewed by 852

Special Issue Editors


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Guest Editor
Key Laboratory for Animal Genetics, Breeding, Reproduction and Molecular Design, College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China
Interests: omics sciences; genetic regulation; gene editing; biological control of mycotoxin; alleviation of toxicity; molecular target identification

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Guest Editor
College of Animal Nutrition and Feed Science, Huazhong Agricultural University, Wuhan 430070, China
Interests: animal nutrition; feed safety; mycotoxins; animal health; selenium
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Special Issue Information

Dear Colleagues,

Mycotoxins frequently occur in fungi-contaminated human food and animal feed, which poses a serious threat to human and animal health. Exposure to mycotoxins can result in a series of toxicities, e.g., immunotoxicity, nephrotoxicity, mutagenicity, hepatotoxicity, etc. Therefore, prevention and control of mycotoxin toxicity are of high importance. Biological control has been proposed as a promising and sustainable strategy to reduce the toxicity of mycotoxins. Identification of the biological agents with alleviative effects of mycotoxin-induced toxicity and elucidation of the molecular mechanisms not only contribute to our understanding of mycotoxin molecular toxicology but also provide supports for the development of strategies against mycotoxin contaminations. The rapid development of molecular biotechnologies and bioinformatics has significantly boosted the research on the alleviation of mycotoxin-induced toxicity, which further promotes the applications of biological agents in reducing or eliminating mycotoxin-induced toxicity.

This Special Issue will publish studies focusing on the detection of biological agents such as plant extracts and small molecules that exhibit alleviative effects on mycotoxin toxicity and on the elucidation of molecular events involved in these biological processes.

Dr. Haifei Wang
Prof. Dr. Lvhui Sun
Guest Editors

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Keywords

  • mycotoxin
  • plant extracts
  • small molecules
  • molecular targets
  • toxicity alleviation
  • molecular toxicology

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Published Papers (3 papers)

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Research

17 pages, 7461 KiB  
Article
Apoptotic Effect of Combinations of T-2, HT-2, and Diacetoxyscirpenol on Human Jurkat T Cells
by Phattarawadee Wattanasuntorn, Saranya Poapolathep, Patchara Phuektes, Imourana Alassane-Kpembi, Johanna Fink-Gremmels, Isabelle P. Oswald and Amnart Poapolathep
Toxins 2025, 17(4), 203; https://doi.org/10.3390/toxins17040203 - 18 Apr 2025
Viewed by 83
Abstract
Trichothecene type A mycotoxins, such as T-2, HT-2, and diacetoxyscirpenol (DAS), are known to induce cytotoxicity and apoptosis in different cell types. As all three Fusarium toxins may occur concomitantly in a given food or feed commodity, there is growing interest in the [...] Read more.
Trichothecene type A mycotoxins, such as T-2, HT-2, and diacetoxyscirpenol (DAS), are known to induce cytotoxicity and apoptosis in different cell types. As all three Fusarium toxins may occur concomitantly in a given food or feed commodity, there is growing interest in the effect of such mycotoxin mixtures. This study aimed to identify the toxic interactions among T-2, HT-2, and DAS in a human Jurkat cell model. As a first step, an MTT assay was used to assess cytotoxicity after 24 h of cell exposure to individual mycotoxins and their mixtures. The results were used to calculate the combination index (CI), which indicates the nature of the mycotoxin interactions. In Jurkat T cells, the toxicity ranking for the individual mycotoxins was T-2 > HT-2 > DAS. The CI values of the dual and triple mycotoxin combinations calculated from the results of the MTT and reactive oxygen species assays showed synergistic effects at low concentrations and an apparent antagonism at very high concentrations for all combinations. The additional cytometric analyses confirmed the synergistic effects, as expected, following co-exposure to the three tested trichothecenes. As the lower toxin concentrations investigated reflect natural contamination levels in food and feeds, the synergistic effects identified should be considered in risk characterization for trichothecene exposure in humans and animals. Full article
(This article belongs to the Special Issue Alleviation of Mycotoxin-Induced Toxicity)
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15 pages, 4041 KiB  
Article
Insights from Metabolomic and Transcriptomic Analyses into Sulforaphane’s Protective Mechanism Against Deoxynivalenol Toxicity via Spermine Regulation
by Yeyi Xiao, Jianliang Wu, Menke Feng, Jie Wang, Lele Qi, Chao Xu, Haifei Wang and Wenbin Bao
Toxins 2025, 17(4), 178; https://doi.org/10.3390/toxins17040178 - 3 Apr 2025
Viewed by 230
Abstract
Deoxynivalenol (DON) is a mycotoxin ubiquitously present in the environment. Emerging evidence demonstrated that sulforaphane (SFN) exerts potent protective effects against DON-triggered cytotoxicity through multimodal mechanisms. This study aimed to investigate the protective mechanism of SFN during DON exposure. Untargeted metabolomics of IPEC-J2 [...] Read more.
Deoxynivalenol (DON) is a mycotoxin ubiquitously present in the environment. Emerging evidence demonstrated that sulforaphane (SFN) exerts potent protective effects against DON-triggered cytotoxicity through multimodal mechanisms. This study aimed to investigate the protective mechanism of SFN during DON exposure. Untargeted metabolomics of IPEC-J2 cells revealed a total of 399 differential metabolites between the DON and control group and 365 differential metabolites between the SFN + DON and DON group. KEGG enrichment was performed to investigate the potential regulatory pathways. The transcriptome identified a total of 1839 differential expression genes (DEGs) between DON and SFN + DON groups. This result indicated that DON exposure and SFN treatment have a profound impact on cellular metabolism and genes. Integrated analysis of the transcriptome and metabolome showed that spermine was a potential biomarker for SFN treatment. SFN increased spermine abundance by regulating genes in glutathione, beta-alanine, and arginine and proline metabolism pathways. Functional experiments demonstrated that spermine alleviated DON-induced oxidative stress, as evidenced by increased cell viability, reduced ROS levels, restored mitochondrial membrane potential (ΔΨm), and normalized antioxidant enzyme activity. Moreover, spermine significantly decreased the cell apoptosis rate induced by DON, which suggested that spermine significantly alleviated the DON-induced cytotoxicity. Overall, these findings elucidated the protective role of SFN through spermine-related mechanisms against the toxicity of DON. Full article
(This article belongs to the Special Issue Alleviation of Mycotoxin-Induced Toxicity)
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13 pages, 2003 KiB  
Article
Ivangustin Alleviates Deoxynivalenol-Induced Apoptosis by Regulating FOXO3a Translocation in Porcine Intestinal Epithelial Cells
by Tae Hong Kang, Sang Su Shin, Tae Hyun Kim and Sang In Lee
Toxins 2025, 17(4), 174; https://doi.org/10.3390/toxins17040174 - 2 Apr 2025
Viewed by 220
Abstract
Deoxynivalenol (DON) is a mycotoxin derived from Fusarium species. It is commonly found in crops and has a high detection rate in animal feedstuffs. We previously confirmed that apoptosis could be induced by DON through the FOXO3a (Forkhead box 3a) signaling pathway. In [...] Read more.
Deoxynivalenol (DON) is a mycotoxin derived from Fusarium species. It is commonly found in crops and has a high detection rate in animal feedstuffs. We previously confirmed that apoptosis could be induced by DON through the FOXO3a (Forkhead box 3a) signaling pathway. In this study, to identify a natural compound to mitigate DON-induced apoptosis via FOXO3a, we performed high-throughput screening. We found that ivangustin (IVAN) alleviated DON-induced cytotoxicity. It also decreased DON-mediated apoptosis and the expression levels of apoptosis-associated genes at the mRNA level. Furthermore, treatment with IVAN inhibited FOXO3a from translocating into the nucleus. The results demonstrated the mitigating effects of the natural compound IVAN on DON-induced apoptosis through the FOXO3a signaling pathway. This study focused on elucidating the mechanism underlying damage caused by DON. According to the results of this study, novel alternatives to mitigate DON cytotoxicity may be developed. This study could provide fundamental data for the formulation of mycotoxin alleviation strategies to improve pig productivity. Full article
(This article belongs to the Special Issue Alleviation of Mycotoxin-Induced Toxicity)
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