Special Issue "Mycotoxins and Their Metabolites Biochemistry, Molecular Biology and Toxicology"

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

Deadline for manuscript submissions: 31 December 2021.

Special Issue Editors

Prof. Dr. Kamil Kuca
E-Mail Website
Guest Editor
1. Center for Basic and Applied Research, Faculty of Informatics and Management, University of Hradec Kralove, 50003 Hradec Kralove, Czech Republic
2. Biomedical Research Center, University Hospital Hradec Kralove, 50005 Hradec Kralove, Czech Republic
Interests: drug design and development; antidotes for pesticide and nerve agent intoxications; Alzheimer’s disease; detergents as disinfectants, decontamination means; toxins; nanotechnology; project management; scientific management; technology transfer; health economics and pharmacoeconomics
Special Issues and Collections in MDPI journals
Prof. Qinghua Wu
E-Mail Website
Guest Editor
College of Life Science, Yangtze University, Jingzhou, China
Interests: toxin; synthetic toxins; natural toxin; toxic industrial chemicals; chemical warfare agents; antidotes; signalling pathway; molecular biology; in vitro & in vivo; biochemistry
Special Issues and Collections in MDPI journals
Dr. Eugenie Nepovimova
E-Mail Website
Guest Editor
Faculty of Science, University of Hradec Kralove, Hradec Kralove, Czech

Special Issue Information

Mycotoxins comprise hundreds of toxic secondary metabolites that are produced by fungi and contaminate cereal grains, leading to serious effects on human and animal health. Pathophysiologic effects associated with mycotoxins include immunosuppression, altered neuroendocrine signaling, proinflammatory gene induction, malnutrition, disruption of the growth hormone axis, carcinogenesis, and reproductive and teratogenic effects. Exposure routes, bioavailability, and potential accumulation of mycotoxins in different species or organs can lead to different toxicities. Although the toxicity of most metabolites has been reduced compared with the original mycotoxins, they are still extremely harmful to humans and animals, suggesting that further investigations into toxicity are necessary. As more and more novel mycotoxins and metabolites are discovered, there is increasing interest in studying the toxicity and molecular mechanisms of these toxins and their major metabolites. This Special Issue of Toxins is focused on new insights and advances in cellular and molecular mechanisms of toxicity induced by mycotoxins and their major metabolites, especially from biochemistry and signaling pathways that underlie these toxic responses. While the focus is on molecular biology and toxicology of mycotoxins and metablites, manuscripts addressing the occurrence, contamination, and risk assessment of novel mycotoxins and metabolites will also be considered.

Prof. Dr. Kamil Kuca
Prof. Qinghua Wu
Dr. Eugenie Nepovimova
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 papers will be 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 double-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxins 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 2400 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
  • metabolites
  • toxicology
  • molecular mechanisms

Published Papers (3 papers)

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Research

Article
Deoxynivalenol (Vomitoxin)-Induced Anorexia Is Induced by the Release of Intestinal Hormones in Mice
Toxins 2021, 13(8), 512; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13080512 - 22 Jul 2021
Viewed by 640
Abstract
Deoxynivalenol (DON), also known as vomitoxin, is a mycotoxin that can cause antifeeding and vomiting in animals. However, the mechanism of DON inducing anorexia is complicated. Studies have shown that intestinal hormones play a significant part in the anorexia caused by DON. We [...] Read more.
Deoxynivalenol (DON), also known as vomitoxin, is a mycotoxin that can cause antifeeding and vomiting in animals. However, the mechanism of DON inducing anorexia is complicated. Studies have shown that intestinal hormones play a significant part in the anorexia caused by DON. We adopted the “modeling of acute antifeeding in mice” as the basic experimental model, and used two methods of gavage and intraperitoneal injection to explore the effect of intestinal hormones on the antifeedant response induced by DON in mice. We found that 1 and 2.5 mg/kg·bw of DON can acutely induce anorexia and increase the plasma intestinal hormones CCK, PYY, GIP, and GLP-1 in mice within 3 h. Direct injection of exogenous intestinal hormones CCK, PYY, GIP, and GLP-1 can trigger anorexia behavior in mice. Furthermore, the PYY receptor antagonist JNJ-31020028, GLP-1 receptor antagonist Exendin(9-39), CCK receptor antagonist Proglumide, GIP receptor antagonist GIP(3-30)NH2 attenuated both intestinal hormone and DON-induced anorectic responses. These results indicate that intestinal hormones play a critical role in the anorexia response induced by DON. Full article
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Article
Antidotal Potency of the Novel, Structurally Different Adsorbents in Rats Acutely Intoxicated with the T-2 Toxin
Toxins 2020, 12(10), 643; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins12100643 - 05 Oct 2020
Cited by 1 | Viewed by 926
Abstract
In this paper, the potential antidote efficacy of commercially available formulations of various feed additives such as Minazel-Plus®, Mycosorb®, and Mycofix® was considered by recording their incidence on general health, body weight, and food and water intake, as [...] Read more.
In this paper, the potential antidote efficacy of commercially available formulations of various feed additives such as Minazel-Plus®, Mycosorb®, and Mycofix® was considered by recording their incidence on general health, body weight, and food and water intake, as well as through histopathology and semiquantitative analysis of gastric alterations in Wistar rats treated with the T-2 toxin in a single-dose regimen of 1.67 mg/kg p.o. (1 LD50) for 4 weeks. As an organic adsorbent, Mycosorb® successfully antagonized acute lethal incidence of the T-2 toxin (protective index (PI) = 2.25; p < 0.05 vs. T-2 toxin), and had adverse effects on body weight gain as well as food and water intake during the research (p < 0.001). However, the protective efficacy of the other two food additives was significantly lower (p < 0.05). Treatment with Mycosorb® significantly reduced the severity of gastric damage, which was not the case when the other two adsorbents were used. Our results suggest that Mycosorb® is a much better adsorbent for preventing the adverse impact of the T-2 toxin as well as its toxic metabolites compared with Minazel-plus® or Mycofix-plus®, and it almost completely suppresses its acute toxic effects and cytotoxic potential on the gastric epithelial, glandular, and vascular endothelial cells. Full article
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Article
Type A Trichothecene Diacetoxyscirpenol-Induced Emesis Corresponds to Secretion of Peptide YY and Serotonin in Mink
Toxins 2020, 12(6), 419; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins12060419 - 25 Jun 2020
Cited by 1 | Viewed by 893
Abstract
The trichothecene mycotoxins contaminate cereal grains and have been related to alimentary toxicosis resulted in emetic response. This family of mycotoxins comprises type A to D groups of toxic sesquiterpene chemicals. Diacetoxyscirpenol (DAS), one of the most toxic type A trichothecenes, is considered [...] Read more.
The trichothecene mycotoxins contaminate cereal grains and have been related to alimentary toxicosis resulted in emetic response. This family of mycotoxins comprises type A to D groups of toxic sesquiterpene chemicals. Diacetoxyscirpenol (DAS), one of the most toxic type A trichothecenes, is considered to be a potential risk for human and animal health by the European Food Safety Authority. Other type A trichothecenes, T-2 toxin and HT-2 toxin, as well as type B trichothecene deoxynivalenol (DON), have been previously demonstrated to induce emetic response in the mink, and this response has been associated with the plasma elevation of neurotransmitters peptide YY (PYY) and serotonin (5-hydroxytryptamine, 5-HT). However, it is found that not all the type A and type B trichothecenes have the capacity to induce PYY and 5-HT. It is necessary to identify the roles of these two emetogenic mediators on DAS-induced emesis. The goal of this study was to determine the emetic effect of DAS and relate this effect to PYY and 5-HT, using a mink bioassay. Briefly, minks were fasted one day before experiment and given DAS by intraperitoneally and orally dosing on the experiment day. Then, emetic episodes were calculated and blood collection was employed for PYY and 5-HT test. DAS elicited robust emetic responses that corresponded to upraised PYY and 5-HT. Blocking the neuropeptide Y2 receptor (NPY2R) diminished emesis induction by PYY and DAS. The serotonin 3 receptor (5-HT3R) inhibitor granisetron totally restrained the induction of emesis by serotonin and DAS. In conclusion, our findings demonstrate that PYY and 5-HT have critical roles in DAS-induced emetic response. Full article
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