Special Issue "The Toxic Effects of Mycotoxins and Underlying Molecular Mechanisms"

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Toxicology".

Deadline for manuscript submissions: 16 October 2022 | Viewed by 551

Special Issue Editor

Dr. Chongshan Dai
E-Mail Website1 Website2
Guest Editor
1. College of Veterinary Medicine, China Agricultural University, Beijing, China
2. Beijing Key Laboratory of Detection Technology for Animal-Derived Food Safety, Beijing, China
3. Key Biology Laboratory of Chinese Veterinary Medicine, Ministry of Agriculture and Rural Affairs, Beijing, China
Interests: antioxidants; oxidative stress; molecular mechanism; autophagy; ferroptosis; neurotoxicity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The secondary metabolites produced by fungi known as mycotoxins are capable of causing mycotoxicosis (diseases and death) in humans and animals. To date, more than 400 mycotoxins have been identified and most of them have exhibited various toxic effects. Nowadays, mycotoxins exposure threatens both animal and human health and have gained widespread concern. According to their toxic effects, mycotoxins are classified as neurotoxins, immunotoxins, hepatotoxins, nephrotoxins, etc. In the past 60 years, the molecular mechanisms of some mycotoxins have gained some progress involving oxidative stress, mitochondrial dysfunction, inflammatory response, immunosuppression, autophagy regulation and apoptotic cell death. However, so far, their critical molecular mechanisms remain largely unknown, which makes it difficult to find effective treatment strategies in a timely manner after mycotoxins poisons are found in humans and animals. Therefore, underlying the precise toxic mechanisms of mycotoxins is essential in the search for effective treatment strategies.

In this Special Issue, we aim to collate innovative original research and review articles that reveal new pathogenic pathways, toxic mechanisms, potential therapeutic strategies, and protective agents, presenting targeting mycotoxins-induced toxic effects in vivo and in vitro.

Dr. Chongshan Dai
Guest Editor

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxics is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • mycotoxins
  • in vivo
  • in vitro
  • toxic mechanisms
  • therapeutic strategies
  • protective agents
  • new pathogenic pathways
  • toxic effects

Published Papers (1 paper)

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Research

Article
Ginsenoside Rg1 Mitigates Porcine Intestinal Tight Junction Disruptions Induced by LPS through the p38 MAPK/NLRP3 Inflammasome Pathway
Toxics 2022, 10(6), 285; https://doi.org/10.3390/toxics10060285 - 27 May 2022
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Abstract
Inflammation leads to porcine tight junction disruption of small intestinal epithelial cells, resulting in intestinal dysfunction. Herein, we established lipopolysaccharide (LPS)-induced in-vivo and in-vitro inflammatory models. The results revealed that LPS induced tight junction disruption in IPEC-J2 cells by downregulating tight-junction-related protein zonula [...] Read more.
Inflammation leads to porcine tight junction disruption of small intestinal epithelial cells, resulting in intestinal dysfunction. Herein, we established lipopolysaccharide (LPS)-induced in-vivo and in-vitro inflammatory models. The results revealed that LPS induced tight junction disruption in IPEC-J2 cells by downregulating tight-junction-related protein zonula occludens-1 (ZO-1), occludin and claudin-1 expression, while ginsenoside Rg1 rescued such inhibition and abrogated the upregulated expression of phosphorylation p38 MAPK. The p38 MAPK inhibitor (SB203580) showed a similar effect with Rg1 and attenuated the LPS-induced inhibition of ZO-1, occludin and claudin-1 expression, which is consistent with the reduced expression of NLRP3 inflammasome and IL-1β. Furthermore, the specific inhibitors of NLRP3 and IL-1β result in increased expression of tight-junction-related protein, demonstrating that p38 MAPK signaling was associated with Rg1 suppression of tight junction disruption. Besides, LPS treatment decreased the expression of ZO-1, occludin and claudin-1 through p38 MAPK signaling, and caused abnormal morphological changes in murine ileum. Meanwhile, Rg1 attenuated the decreased expression of ZO-1, occludin and claudin-1 and partially alleviated LPS-induced morphological changes in murine ileum. In summary, these findings characterized a novel mechanism by which Rg1 alleviates LPS-induced intestinal tight junction disruption by inhibiting the p38 MAPK-mediated NLRP3 inflammasome pathway. Full article
(This article belongs to the Special Issue The Toxic Effects of Mycotoxins and Underlying Molecular Mechanisms)
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