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Toxics
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The Toxic Effects of Mycotoxins and Underlying Molecular Mechanisms
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The Toxic Effects of Mycotoxins and Underlying Molecular Mechanisms

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

Deadline for manuscript submissions: closed (16 May 2023) | Viewed by 11102

Special Issue Editor

Dr. Chongshan Dai

E-Mail Website
Guest Editor
Department of Veterinary Pharmacology and Toxicology, College of Veterinary Medicine, China Agricultural University, No. 2 Yuanmingyuan West Road, Beijing 100193, 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

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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 2600 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 (4 papers)

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Research

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12 pages, 2276 KiB  
Article
Ginsenoside Rg1 Mitigates Porcine Intestinal Tight Junction Disruptions Induced by LPS through the p38 MAPK/NLRP3 Inflammasome Pathway
by Jian Kang, Yanhong Zhou, Chunyang Zhu, Tian Ren, Yong Zhang, Longfei Xiao and Binghu Fang
Toxics 2022, 10(6), 285; https://doi.org/10.3390/toxics10060285 - 27 May 2022
Cited by 4 | Viewed by 2740
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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Review

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15 pages, 1638 KiB  
Review
Ferroptosis as a Potential Therapeutic Target of Traditional Chinese Medicine for Mycotoxicosis: A Review
by Wenli Ding, Luxi Lin, Ke Yue, Yanfeng He, Bowen Xu, Aftab Shaukat and Shucheng Huang
Toxics 2023, 11(4), 395; https://doi.org/10.3390/toxics11040395 - 21 Apr 2023
Cited by 5 | Viewed by 1964
Abstract
Mycotoxin contamination has become one of the biggest hidden dangers of food safety, which seriously threatens human health. Understanding the mechanisms by which mycotoxins exert toxicity is key to detoxification. Ferroptosis is an adjustable cell death characterized by iron overload and lipid reactive [...] Read more.
Mycotoxin contamination has become one of the biggest hidden dangers of food safety, which seriously threatens human health. Understanding the mechanisms by which mycotoxins exert toxicity is key to detoxification. Ferroptosis is an adjustable cell death characterized by iron overload and lipid reactive oxygen species (ROS) accumulation and glutathione (GSH) depletion. More and more studies have shown that ferroptosis is involved in organ damage from mycotoxins exposure, and natural antioxidants can alleviate mycotoxicosis as well as effectively regulate ferroptosis. In recent years, research on the treatment of diseases by Chinese herbal medicine through ferroptosis has attracted more attention. This article reviews the mechanism of ferroptosis, discusses the role of ferroptosis in mycotoxicosis, and summarizes the current status of the regulation of various mycotoxicosis through ferroptosis by Chinese herbal interventions, providing a potential strategy for better involvement of Chinese herbal medicine in the treatment of mycotoxicosis in the future. Full article
(This article belongs to the Special Issue The Toxic Effects of Mycotoxins and Underlying Molecular Mechanisms)
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17 pages, 3122 KiB  
Review
Nrf2: A Main Responsive Element of the Toxicity Effect Caused by Trichothecene (T-2) Mycotoxin
by Youshuang Wang, Yu Liu, Tingyu Huang, Yunhe Chen, Wenxi Song, Fengjuan Chen, Yibao Jiang, Cong Zhang and Xu Yang
Toxics 2023, 11(4), 393; https://doi.org/10.3390/toxics11040393 - 21 Apr 2023
Cited by 4 | Viewed by 1446
Abstract
T-2 toxin, the most toxic type A trichothecene mycotoxin, is produced by Fusarium, and is widely found in contaminated feed and stored grains. T-2 toxin is physicochemically stable and is challenging to eradicate from contaminated feed and cereal, resulting in food contamination that [...] Read more.
T-2 toxin, the most toxic type A trichothecene mycotoxin, is produced by Fusarium, and is widely found in contaminated feed and stored grains. T-2 toxin is physicochemically stable and is challenging to eradicate from contaminated feed and cereal, resulting in food contamination that is inescapable and poses a major hazard to both human and animal health, according to the World Health Organization. Oxidative stress is the upstream cause of all pathogenic variables, and is the primary mechanism through which T-2 toxin causes poisoning. Nuclear factor E2-related factor 2 (Nrf2) also plays a crucial part in oxidative stress, iron metabolism and mitochondrial homeostasis. The major ideas and emerging trends in future study are comprehensively discussed in this review, along with research progress and the molecular mechanism of Nrf2’s involvement in the toxicity impact brought on by T-2 toxin. This paper could provide a theoretical foundation for elucidating how Nrf2 reduces oxidative damage caused by T-2 toxin, and a theoretical reference for exploring target drugs to alleviate T-2 toxin toxicity with Nrf2 molecules. Full article
(This article belongs to the Special Issue The Toxic Effects of Mycotoxins and Underlying Molecular Mechanisms)
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15 pages, 19538 KiB  
Review
Plant Resistance to Fungal Pathogens: Bibliometric Analysis and Visualization
by Yueyue Tang, Guandi He, Yeqing He and Tengbing He
Toxics 2022, 10(10), 624; https://doi.org/10.3390/toxics10100624 - 19 Oct 2022
Cited by 2 | Viewed by 4338
Abstract
Plants are susceptible to fungal pathogen infection, threatening plant growth and development. Researchers worldwide have conducted extensive studies to address this issue and have published numerous articles on the subject, but they lack a scientometric evaluation. This study analyzed international research on the [...] Read more.
Plants are susceptible to fungal pathogen infection, threatening plant growth and development. Researchers worldwide have conducted extensive studies to address this issue and have published numerous articles on the subject, but they lack a scientometric evaluation. This study analyzed international research on the topic “Plant resistance to fungal pathogens” between 2008 and 2021, using the core database of the Web of Science (WoS). By searching the subject words “Plants”, “Disease Resistance”, and “Fungal Pathogens”, we received 6687 articles. Bibliometric visualization software analyzes the most published countries, institutions, journals, authors, the most cited articles, and the most common keywords. The results show that the number of articles in the database has increased year by year, with the United States and China occupying the core positions, accounting for 46.16% of the total published articles worldwide. The United States Department of Agriculture (USDA) is the main publishing organization. Wang Guoliang is the author with the most published articles, and the Frontiers in Plant Science ranks first in published articles. The research on plant anti-fungal pathogens is booming, and international exchanges and cooperation need to be further strengthened. This paper summarizes five possible research ideas, from fungal pathogens, gene editing technology, extraction of secondary metabolites from plants as anti-fungal agents, identification of related signal pathways, fungal molecular databases, and development of nanomaterials, to provide data for related research. Full article
(This article belongs to the Special Issue The Toxic Effects of Mycotoxins and Underlying Molecular Mechanisms)
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