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Toxins
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Mycotoxins and Their Metabolites Biochemistry, Molecular Biology and Toxicology
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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: closed (31 December 2021) | Viewed by 16004

Special Issue Editors

Prof. Dr. Kamil Kuca

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Guest Editor
Department of Chemistry, Faculty of Science, University of Hradec Králové, 50003 Hradec Králové, Czech Republic
Interests: toxins; drug design and development; antidotes for pesticide and nerve agent intoxications; Alzheimer’s disease; detergents as disinfectants, decontamination means; nanotechnology; health economics and pharmacoeconomics
Special Issues, Collections and Topics 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, Collections and Topics in MDPI journals
Dr. Eugenie Nepovimova

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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 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 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 2700 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 (6 papers)

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Research

13 pages, 12677 KiB  
Article
Comparative Cytotoxic Effects and Possible Mechanisms of Deoxynivalenol, Zearalenone and T-2 Toxin Exposure to Porcine Leydig Cells In Vitro
by Lingwei Sun, Jianjun Dai, Jiehuan Xu, Junhua Yang and Defu Zhang
Toxins 2022, 14(2), 113; https://doi.org/10.3390/toxins14020113 - 02 Feb 2022
Cited by 11 | Viewed by 2068
Abstract
Mycotoxins such as zearalenone (ZEN), deoxynivalenol (DON) and T-2 toxin (T-2) are the most poisonous biological toxins in food pollution. Mycotoxin contaminations are a global health issue. The aim of the current study was to use porcine Leydig cells as a model to [...] Read more.
Mycotoxins such as zearalenone (ZEN), deoxynivalenol (DON) and T-2 toxin (T-2) are the most poisonous biological toxins in food pollution. Mycotoxin contaminations are a global health issue. The aim of the current study was to use porcine Leydig cells as a model to explore the toxic effects and underlying mechanisms of ZEN, DON and T-2. The 50% inhibitory concentration (IC50) of ZEN was 49.71 μM, and the IC50 values of DON and T-2 were 2.49 μM and 97.18 nM, respectively. Based on the values of IC50, ZEN, DON and T-2 exposure resulted in increased cell apoptosis, as well as disrupted mitochondria membrane potential and cell cycle distribution. The results also showed that ZEN and DON significantly reduced testosterone and progesterone secretion in Leydig cells, but T-2 only reduced testosterone secretion. Furthermore, the expression of steroidogenic acute regulatory (StAR) protein and 3β-hydroxysteroid dehydrogenase (3β-HSD) were significantly decreased by ZEN, DON and T-2; whereas the protein expression of cholesterol side-chain cleavage enzyme (CYP11A1) was only significantly decreased by ZEN. Altogether, these data suggest that the ZEN, DON and T-2 toxins resulted in reproductive toxicity involving the inhibition of steroidogenesis and cell proliferation, which contributes to the cellular apoptosis induced by mitochondrial injury in porcine Leydig cells. Full article
(This article belongs to the Special Issue Mycotoxins and Their Metabolites Biochemistry, Molecular Biology and Toxicology)
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13 pages, 4605 KiB  
Article
Zearalenone Exposure Triggered Cecal Physical Barrier Injury through the TGF-β1/Smads Signaling Pathway in Weaned Piglets
by Pengfei Zhang, Changwei Jing, Ming Liang, Shuzhen Jiang, Libo Huang, Ning Jiao, Yang Li and Weiren Yang
Toxins 2021, 13(12), 902; https://doi.org/10.3390/toxins13120902 - 15 Dec 2021
Cited by 12 | Viewed by 2431
Abstract
This study aims to investigate the effects of exposure to different dosages of zearalenone (ZEA) on cecal physical barrier functions and its mechanisms based on the TGF-β1/Smads signaling pathway in weaned piglets. Thirty-two weaned piglets were allotted to four groups and fed a [...] Read more.
This study aims to investigate the effects of exposure to different dosages of zearalenone (ZEA) on cecal physical barrier functions and its mechanisms based on the TGF-β1/Smads signaling pathway in weaned piglets. Thirty-two weaned piglets were allotted to four groups and fed a basal diet supplemented with ZEA at 0, 0.15, 1.5, and 3.0 mg/kg, respectively. The results showed that 1.5 and 3.0 mg/kg ZEA damaged cecum morphology and microvilli, and changed distribution and shape of M cells. Moreover, 1.5 and 3.0 mg/kg ZEA decreased numbers of goblet cells, the expressions of TFF3 and tight junction proteins, and inhibited the TGF-β1/Smads signaling pathway. Interestingly, the 0.15 mg/kg ZEA had no significant effect on cecal physical barrier functions but decreased the expressions of Smad3, p-Smad3 and Smad7. Our study suggests that high-dose ZEA exposure impairs cecal physical barrier functions through inhibiting the TGF-β1/Smads signaling pathway, but low-dose ZEA had no significant effect on cecum morphology and integrity through inhibiting the expression of smad7. These findings provide a scientific basis for helping people explore how to reduce the toxicity of ZEA in feeds. Full article
(This article belongs to the Special Issue Mycotoxins and Their Metabolites Biochemistry, Molecular Biology and Toxicology)
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15 pages, 3454 KiB  
Article
The Protective Effect of Heme Oxygenase-1 on Liver Injury Caused by DON-Induced Oxidative Stress and Cytotoxicity
by Zitong Meng, Liangliang Wang, Yuxiao Liao, Zhao Peng, Dan Li, Xiaolei Zhou, Shuang Liu, Yanmei Li, Andreas K. Nüssler, Liegang Liu, Liping Hao and Wei Yang
Toxins 2021, 13(10), 732; https://doi.org/10.3390/toxins13100732 - 17 Oct 2021
Cited by 8 | Viewed by 2891
Abstract
Deoxynivalenol (DON) is a kind of Fusarium toxin that can cause a variety of toxic effects. Oxidative stress and DNA damage play a critical role in the toxicity of DON. However, previous studies focused more on acute toxicity in vivo/vitro models and lacked [...] Read more.
Deoxynivalenol (DON) is a kind of Fusarium toxin that can cause a variety of toxic effects. Oxidative stress and DNA damage play a critical role in the toxicity of DON. However, previous studies focused more on acute toxicity in vivo/vitro models and lacked subchronic toxicity study in vivo. The potentially harmful effect of DON given at doses comparable to the daily human consumption in target organs, especially the liver, which is the main detoxification organ of DON, is also still not fully understood. Otherwise, Heme Oxygenase-1 (HO-1) has also reduced cell damage under the DON condition according to our previous study. Therefore, we used a rodent model that mimicked daily human exposure to DON and further explored its mechanism of toxic effects on liver tissue and Hepa 1–6 cell line. We also used adeno-associated virus (AAV)-modified HO-1 expressing by tail vein injection and constructed lentivirus-Hepa 1–6 cell line for mimicking HO-1 protective ability under the DON condition. The main results showed that both 30 d and 90 d exposures of DON could cause low-grade inflammatory infiltration around hepatic centrilobular veins. The reactive oxygen species (ROS) and 8-hydroxy-2 deoxyguanosine (8-OHdG) increased during DON exposure, indicating oxidation stress and DNA damage. Significantly, AAV-mediated liver-specific overexpression of HO-1 reduced DON-induced liver damage and indirectly protected the abilities of antioxidant enzyme/DNA damage repair system, while AAV-mediated silence of HO-1 produced the opposite effect. In addition, we found that overexpression of HO-1 could enhance autophagy and combined it with an antioxidant enzyme/DNA damage repair system to inhibit DON-induced hepatocyte damage. Altogether, these data suggest that HO-1 reduces the oxidative stress and DNA damage caused by DON sub-chronic exposure through maintaining DNA repair, antioxidant activity, as well as autophagy. Full article
(This article belongs to the Special Issue Mycotoxins and Their Metabolites Biochemistry, Molecular Biology and Toxicology)
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14 pages, 2139 KiB  
Article
Deoxynivalenol (Vomitoxin)-Induced Anorexia Is Induced by the Release of Intestinal Hormones in Mice
by Jianming Yue, Dawei Guo, Xiuge Gao, Jiacai Wang, Eugenie Nepovimova, Wenda Wu and Kamil Kuca
Toxins 2021, 13(8), 512; https://doi.org/10.3390/toxins13080512 - 22 Jul 2021
Cited by 9 | Viewed by 2468
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
(This article belongs to the Special Issue Mycotoxins and Their Metabolites Biochemistry, Molecular Biology and Toxicology)
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15 pages, 2942 KiB  
Article
Antidotal Potency of the Novel, Structurally Different Adsorbents in Rats Acutely Intoxicated with the T-2 Toxin
by Vesna Jaćević, Jelena Dumanović, Miodrag Lazarević, Eugenie Nepovimova, Radmila Resanović, Zoran Milovanović, Qinghua Wu and Kamil Kuča
Toxins 2020, 12(10), 643; https://doi.org/10.3390/toxins12100643 - 05 Oct 2020
Cited by 8 | Viewed by 2692
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
(This article belongs to the Special Issue Mycotoxins and Their Metabolites Biochemistry, Molecular Biology and Toxicology)
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12 pages, 2193 KiB  
Article
Type A Trichothecene Diacetoxyscirpenol-Induced Emesis Corresponds to Secretion of Peptide YY and Serotonin in Mink
by Qinghua Wu, Kamil Kuca, Eugenie Nepovimova and Wenda Wu
Toxins 2020, 12(6), 419; https://doi.org/10.3390/toxins12060419 - 25 Jun 2020
Cited by 10 | Viewed by 2512
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
(This article belongs to the Special Issue Mycotoxins and Their Metabolites Biochemistry, Molecular Biology and Toxicology)
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