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The Metabolism and Cytotoxicity of Mycotoxins: A Threat or a...
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The Metabolism and Cytotoxicity of Mycotoxins: A Threat or a Treat?

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

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 4782

Special Issue Editors

Prof. Dr. Weaam Ebrahim

E-Mail Website
Guest Editor
Department of Pharmacognosy, Faculty of Pharmacy, Mansoura University, El Gomhoria Street 60, Mansoura P.O. Box 35516, Egypt
Interests: microbial natural products; bioactivity; NMR spectroscopy
Prof. Dr. Sherif Ebada

E-Mail Website
Guest Editor
1. Department of Microbial Drugs, Helmholtz Center for Infection Research, 38124 Braunschweig, Germany
2. Department of Pharmacognosy, Faculty of Pharmacy, Ain Shams University, Cairo 11566, Egypt
Interests: fungal secondary metabolites; cytotoxicity; antibiofilm; antimicrobial; structure elucidation

Special Issue Information

Dear Colleagues,

The worldwide contamination of foods and feeds with mycotoxins is a significant problem. Mycotoxins are secondary metabolites of molds that have adverse effects on humans, animals, and crops that result in illnesses and economic losses. In recent years, mycotoxin poisoning has occurred frequently and caused great losses, which makes it particularly important to conduct further research. Many researchers have explored metabolic research on mycotoxins focusing on four classes of toxins: aflatoxins, trichothecenes, zearalenone, and fumonisin.

Cytotoxicity is one of the most important adverse properties of mycotoxins, which may result in cell damage and/or cell death. Therefore, a better understanding of the cytotoxicity and metabolism of mycotoxins is necessary to avoid problems caused by mycotoxins, and to minimize their negative effects on agriculture and health. To date, mycotoxins have inspired the development a number of approved pharmaceuticals. Given this context, we welcome experts and scholars from around the world to share their research outcomes regarding bioactivities exhibited by mycotoxins.

Prof. Dr. Weaam Ebrahim
Prof. Dr. Sherif Ebada
Guest Editors

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
  • metabolism
  • cell damage
  • cytotoxicity
  • toxicology
  • cancer induction

Published Papers (3 papers)

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Research

16 pages, 3846 KiB  
Article
MiR-155-5p Elevated by Ochratoxin A Induces Intestinal Fibrosis and Epithelial-to-Mesenchymal Transition through TGF-β Regulated Signaling Pathway In Vitro and In Vivo
by Kyu Hyun Rhee, Seon Ah Yang, Min Cheol Pyo, Jae-Min Lim and Kwang-Won Lee
Toxins 2023, 15(7), 473; https://doi.org/10.3390/toxins15070473 - 22 Jul 2023
Cited by 5 | Viewed by 1289
Abstract
Ochratoxin A (OTA) is a mycotoxin that induces fibrosis and epithelial-to-mesenchymal transitions (EMT) in kidneys and livers. It enters our bodies through food consumption, where it is absorbed in the intestines. However, the impact of OTA on the intestines is yet to be [...] Read more.
Ochratoxin A (OTA) is a mycotoxin that induces fibrosis and epithelial-to-mesenchymal transitions (EMT) in kidneys and livers. It enters our bodies through food consumption, where it is absorbed in the intestines. However, the impact of OTA on the intestines is yet to be studied. MicroRNA (miRNAs) are small non-coding single-stranded RNAs that block the transcription of specific mRNAs and are, therefore, involved in many biochemical processes. Our findings indicate that OTA can induce EMT and intestinal fibrosis both in vivo and in vitro. This study examines the impact of OTA on intestinal toxicity and the role of miRNAs in this process. Following OTA treatment, miR-155-5p was the most elevated miRNA by next-generation sequencing. Our research showed that OTA increased miR-155-5p levels through transforming growth factor β (TGF-β), leading to the development of intestinal fibrosis and EMT. Additionally, the study identified that the modulation of TGF-β and miR-155-5p by OTA is linked to the inhibition of CCAAT/enhancer-binding protein β (C/EBPβ) and Smad2/3 accumulation in the progression of intestinal fibrosis. Full article
(This article belongs to the Special Issue The Metabolism and Cytotoxicity of Mycotoxins: A Threat or a Treat?)
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12 pages, 4879 KiB  
Article
Combination of Zearalenone and Deoxynivalenol Induces Apoptosis by Mitochondrial Pathway in Piglet Sertoli Cells: Role of Endoplasmic Reticulum Stress
by Sirao Hai, Jiawen Chen, Li Ma, Chenlong Wang, Chuangjiang Chen, Sajid Ur Rahman, Chang Zhao, Shibin Feng, Jinjie Wu and Xichun Wang
Toxins 2023, 15(7), 471; https://doi.org/10.3390/toxins15070471 - 21 Jul 2023
Cited by 3 | Viewed by 1470
Abstract
Zearalenone (ZEA) and deoxynivalenol (DON) are widely found in various feeds, which harms livestock’s reproductive health. Both mitochondria and endoplasmic reticulum (ER) can regulate cell apoptosis. This study aimed to explore the regulatory mechanism of endoplasmic reticulum stress (ERS) on ZEA- combined with [...] Read more.
Zearalenone (ZEA) and deoxynivalenol (DON) are widely found in various feeds, which harms livestock’s reproductive health. Both mitochondria and endoplasmic reticulum (ER) can regulate cell apoptosis. This study aimed to explore the regulatory mechanism of endoplasmic reticulum stress (ERS) on ZEA- combined with DON-induced mitochondrial pathway apoptosis in piglet Sertoli cells (SCs). The results showed that ZEA + DON damaged the ultrastructure of the cells, induced apoptosis, decreased mitochondrial membrane potential, promoted the expression of cytochrome c (CytC), and decreased the cell survival rate. Furthermore, ZEA + DON increased the relative mRNA and protein expression of Bid, Caspase-3, Drp1, and P53, while that of Bcl-2 and Mfn2 declined. ZEA + DON was added after pretreatment with 4-phenylbutyric acid (4-PBA). The results showed that 4-PBA could alleviate the toxicity of ZEA + DON toward SCs. Compared with the ZEA + DON group, 4-PBA improved the cell survival rate, decreased the apoptosis rate, inhibited CytC expression, and increased mitochondrial membrane potential, and the damage to the cell ultrastructure was alleviated. Moreover, after pretreatment with 4-PBA, the relative mRNA and protein expression of Bid, Caspase-3, Drp1, and P53 were downregulated, while the relative mRNA and protein expression of Bcl-2 and Mfn2 were upregulated. It can be concluded that ERS plays an important part in the apoptosis of SCs co-infected with ZEA-DON through the mitochondrial apoptosis pathway, and intervention in this process can provide a new way to alleviate the reproductive toxicity of mycotoxins. Full article
(This article belongs to the Special Issue The Metabolism and Cytotoxicity of Mycotoxins: A Threat or a Treat?)
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15 pages, 3228 KiB  
Article
Emodin, an Emerging Mycotoxin, Induces Endoplasmic Reticulum Stress-Related Hepatotoxicity through IRE1α–XBP1 Axis in HepG2 Cells
by Su Been Park, Gun Hee Cho, Young Eun Park and Hyang Sook Chun
Toxins 2023, 15(7), 455; https://doi.org/10.3390/toxins15070455 - 12 Jul 2023
Cited by 1 | Viewed by 1390
Abstract
Emodin, an emerging mycotoxin, is known to be hepatotoxic, but its mechanism remains unclear. We hypothesized that emodin could induce endoplasmic reticulum (ER) stress through the inositol-requiring enzyme 1 alpha (IRE1α)–X-box-binding protein 1 (XBP1) pathway and apoptosis, which are closely correlated and contribute [...] Read more.
Emodin, an emerging mycotoxin, is known to be hepatotoxic, but its mechanism remains unclear. We hypothesized that emodin could induce endoplasmic reticulum (ER) stress through the inositol-requiring enzyme 1 alpha (IRE1α)–X-box-binding protein 1 (XBP1) pathway and apoptosis, which are closely correlated and contribute to hepatotoxicity. To test this hypothesis, a novel IRE1α inhibitor, STF-083010, was used. An MTT assay was used to evaluate metabolic activity, and quantitative PCR and western blotting were used to investigate the gene and protein expression of ER stress or apoptosis-related markers. Apoptosis was evaluated with flow cytometry. Results showed that emodin induced cytotoxicity in a dose-dependent manner in HepG2 cells and upregulated the expression of binding immunoglobulin protein (BiP), C/EBP homologous protein (CHOP), IRE1α, spliced XBP1, the B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax)/Bcl-2 ratio, and cleaved caspase-3. Cotreatment with emodin and STF-083010 led to the downregulation of BiP and upregulation of CHOP, the Bax/Bcl-2 ratio, and cleaved caspase-3 compared with single treatment with emodin. Furthermore, the apoptosis rate was increased in a dose-dependent manner with emodin treatment. Thus, emodin induced ER stress in HepG2 cells by activating the IRE1α–XBP1 axis and induced apoptosis, indicating that emodin can cause hepatotoxicity. Full article
(This article belongs to the Special Issue The Metabolism and Cytotoxicity of Mycotoxins: A Threat or a Treat?)
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