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Toxins
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Adverse Effects of Co-Contaminated Mycotoxins and Strategies for Their Mitigation
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Adverse Effects of Co-Contaminated Mycotoxins and Strategies for Their Mitigation

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

Deadline for manuscript submissions: 30 September 2026 | Viewed by 10357

Special Issue Editors

Dr. Wence Wang

E-Mail Website
Guest Editor
College of Animal Science, South China Agricultural University, Guangzhou 510642, China
Interests: mycotoxins; animal injury; toxic mechanism; intestinal microbiota
Dr. Mengmeng Li

E-Mail Website
Guest Editor
School of Agricultural Science and Engineering, Liaocheng University, Liaocheng 252000, China
Interests: toxin; livestock products; toxic mechanism; intestinal microbiota

Special Issue Information

Dear Colleagues,

Mycotoxin contamination in feed poses a significant challenge to the global livestock and feed industries. The majority of mycotoxin poisonings in livestock and poultry result from prolonged ingestion of low levels of mycotoxin contaminants, leading to chronic symptoms such as stunted growth, reduced feed efficiency, and diminished productivity. In recent years, greater attention has been given to the presence of multiple mycotoxins in feeds. The combined effects of these toxins can have more severe repercussions on animal health and performance compared to single mycotoxins. Typically, feeds are contaminated with various combinations of aflatoxins, fumonisin, vomitoxin, ochratoxin, and zearalenone. The coexistence and interaction among multiple mycotoxins can generate specific toxic effects with synergistic or additive impacts. These not only contribute to carcinogenesis, teratogenesis, and liver and kidney toxicity in livestock and poultry but also pose a serious threat to the quality of their products as well as human health through the reproductive system and food chain. Therefore, it is crucial not to underestimate the risk posed by exposure to multiple mycotoxins in animals. Further investigation into these aspects is warranted. As technology continues to advance rapidly, it becomes imperative that we employ multi-omics approaches along with other research methods for deeper exploration into the specific mechanisms underlying injury caused by multiple mycotoxins while seeking new additives that effectively mitigate contamination from these toxins. This Special Issue aims to present a series of cutting-edge research articles focusing on combination mycotoxins within this field. We sincerely invite you to submit relevant research or review articles for consideration in this Special Issue.

Dr. Wence Wang
Dr. Mengmeng Li
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 250 words) can be sent to the Editorial Office for assessment.

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

  • co-contaminated mycotoxins
  • mechanisms of toxicity
  • mitigation strategies

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Published Papers (6 papers)

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Research

Jump to: Review

21 pages, 2752 KB  
Article
Nicotinamide Ameliorates Deoxynivalenol-Induced Injury in Renal Cells via Inhibiting PARP1 Hyperactivation and Restoring NAD+ Homeostasis
by Chao Chen, Yifan Qin, Zijun Luo, Peiqiang Mu, Jikai Wen and Yiqun Deng
Toxins 2026, 18(5), 227; https://doi.org/10.3390/toxins18050227 - 10 May 2026
Viewed by 181
Abstract
Deoxynivalenol (DON) is a globally prevalent mycotoxin that threatens food and feed safety via severe multi-organ toxicity. Previous studies indicate that DON induces cellular energy metabolism dysregulation by triggering oxidative stress and impairing mitochondrial function. During this process, nicotinamide adenine dinucleotide (NAD+ [...] Read more.
Deoxynivalenol (DON) is a globally prevalent mycotoxin that threatens food and feed safety via severe multi-organ toxicity. Previous studies indicate that DON induces cellular energy metabolism dysregulation by triggering oxidative stress and impairing mitochondrial function. During this process, nicotinamide adenine dinucleotide (NAD+), a central coenzyme in cellular energy metabolism, frequently exhibits significantly decreased intracellular levels or even complete depletion. However, the molecular mechanisms underlying the disruption of NAD+ homeostasis by DON exposure, as well as the development of targeted countermeasures, remain elusive. Using human embryonic kidney 293T (HEK293T) cells as an in vitro renal toxicity model, we dissected DON-induced NAD+ dysregulation and evaluated the protective potential of nicotinamide (NAM). DON caused significant NAD+ depletion in porcine serum (in vivo) and HEK293T cells (in vitro), which was confirmed as a key driver of cytotoxicity. Mechanistically, although DON binds and inhibits nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme of the NAD+ salvage pathway, neither NAMPT knockdown and overexpression nor nicotinamide mononucleotide (NMN) supplementation rescued DON-induced toxicity. Instead, DON dose-dependently activated poly(ADP-ribose) polymerase 1 (PARP1), the primary intracellular NAD+-consuming enzyme, to accelerate NAD+ depletion. PARP1 knockdown markedly attenuated DON-induced cytotoxicity, identifying PARP1 hyperactivation as the core toxic mechanism. NAM dose-dependently suppressed PARP1 activity, replenished NAD+ pools, and reversed cell injury. These findings establish PARP1-driven NAD+ depletion as an important mechanism of DON-induced renal toxicity, providing a promising intervention candidate for mitigating DON toxicity in food safety. Full article
(This article belongs to the Special Issue Adverse Effects of Co-Contaminated Mycotoxins and Strategies for Their Mitigation)
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16 pages, 5486 KB  
Article
Effects of Zearalenone on the Kiss1/GPR54 System and Related Genes Expression in the Hypothalamus and Pituitary Gland of Weaned Gilts
by Zixue Yuan, Min Zhou, Yue Luan, Lei Kong, Weiren Yang and Shuzhen Jiang
Toxins 2026, 18(5), 195; https://doi.org/10.3390/toxins18050195 - 22 Apr 2026
Viewed by 396
Abstract
Zearalenone (ZEA) is a potent estrogenic mycotoxin known to disrupt reproductive functions, but its precise central neuroendocrine mechanisms remain unclear. This study investigated the effects of ZEA on the hypothalamic-pituitary Kiss1/GPR54 signaling pathway in weaned gilts. A total of 32 gilts were randomly [...] Read more.
Zearalenone (ZEA) is a potent estrogenic mycotoxin known to disrupt reproductive functions, but its precise central neuroendocrine mechanisms remain unclear. This study investigated the effects of ZEA on the hypothalamic-pituitary Kiss1/GPR54 signaling pathway in weaned gilts. A total of 32 gilts were randomly assigned to four dietary treatments contained with 0, 0.15, 1.5, or 3.0 mg/kg ZEA for a 32-day feeding trial. Histopathology, immunohistochemistry, and mRNA/protein expression analyses of GPR30, Kiss1, GPR54, GnRH, and GnRHR in the hypothalamus and pituitary gland were conducted. ZEA exposure induced significant histological damage in both tissues. In the hypothalamus, Kiss1, GPR54, GnRH, and GnRHR exhibited a non-linear response, increasing at moderate doses and decreasing at 3.0 mg/kg ZEA, whereas GPR30 expression was continuously upregulated. In the pituitary gland, GnRHR showed a similar non-linear pattern. Furthermore, high-dose ZEA down-regulated pituitary Kiss1 and GPR54 while up-regulating GnRH and GPR30 expressions. In conclusion, ZEA induces reproductive neuroendocrine toxicity through a complex, dose-dependent modulation of the Kiss1/GPR54 signaling axis. The persistent upregulation of GPR30 suggests it acts as a crucial mediator in disrupting this endocrine feedback loop within the hypothalamus and pituitary gland. Full article
(This article belongs to the Special Issue Adverse Effects of Co-Contaminated Mycotoxins and Strategies for Their Mitigation)
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16 pages, 3064 KB  
Article
Curcumin Mitigates Fumonisin B1-Induced Ovarian Toxicity in Peak-Laying Ducks via Hormone Metabolic Protection and Enhanced Reproductive Resilience
by Lihua Wang, Rui Liang, Qingyun Cao, Zhiwei Hou, Ali Mujtaba Shah, Qiuyi Deng, Xue Li, Jinze Li, Jiaqing Chen, Lukuyu A. Bernard, Muhammad Kashif Saleemi, Lin Yang and Wence Wang
Toxins 2026, 18(1), 34; https://doi.org/10.3390/toxins18010034 - 9 Jan 2026
Cited by 1 | Viewed by 719
Abstract
The objective of this study was to evaluate the protective effect of curcumin (Cur) on reproductive toxicity induced by fumonisin B1 (FB1) in laying ducks during the peak egg-laying period. A total of seventy-two 50-week-old Cherry Valley ducks were randomly [...] Read more.
The objective of this study was to evaluate the protective effect of curcumin (Cur) on reproductive toxicity induced by fumonisin B1 (FB1) in laying ducks during the peak egg-laying period. A total of seventy-two 50-week-old Cherry Valley ducks were randomly assigned to four groups: control, FB1 (30 mg/kg), Cur (200 mg/kg), and Cur + FB1 (200 mg/kg + 30 mg/kg). The experiment lasted for 35 days. Our results showed that cur supplementation effectively restored the reductions in final body weight (p = 0.005) and oviduct length (p = 0.020) induced by FB1 exposure. Residual FB1 concentrations in serum, liver, and ovaries were markedly increased in the FB1-treated group, while Cur significantly decreased the FB1 residual in duck liver (p < 0.05). Meanwhile, Cur supplementation markedly counteracted the FB1-induced reductions in serum total protein, albumin, triglycerides, and high-density lipoprotein induced by FB1 exposure. Cur supplementation effectively regulated FB1-induced oxidative stress, inflammation, and endocrine disruption. Specifically, Cur lowered FB1-induced malondialdehyde levels (p < 0.010), attenuated interleukin-1β increase (p = 0.083), and reversed the reduction in immunoglobulin G levels. FB increased the levels of hormones associated with duck reproduction, including estradiol, follicle-stimulating hormone, and luteinizing hormone; in contrast, curcumin supplementation decreased the levels of these hormones (p < 0.010). Histopathological analysis revealed that Cur significantly alleviated the inflammation and necrosis in the liver, kidneys, ovaries, and oviducts induced by FB1. In conclusion, dietary Cur supplementation effectively alleviated FB1-induced reproductive toxicity in laying ducks by enhancing antioxidant capacity, improving lipid metabolism, and restoring hormonal homeostasis. Full article
(This article belongs to the Special Issue Adverse Effects of Co-Contaminated Mycotoxins and Strategies for Their Mitigation)
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19 pages, 347 KB  
Article
Functional Efficacies of Humate and β-Mannanase Against Aflatoxin B1 and Deoxynivalenol in the Diets for Nursery Pigs
by Yesid R. Garavito-Duarte, Jeonghyeon Son, Alexandra C. Weaver and Sung Woo Kim
Toxins 2025, 17(9), 456; https://doi.org/10.3390/toxins17090456 - 11 Sep 2025
Viewed by 1057
Abstract
After in vitro mycotoxin binding validation, humate and β-mannanase were tested for mitigating the negative effects of aflatoxin B1 and deoxynivalenol. Gilts at 8.7 ± 0.5 kg body weight were allotted to four treatments: NC (uncontaminated diet); PC (contaminated diet: 150 µg [...] Read more.
After in vitro mycotoxin binding validation, humate and β-mannanase were tested for mitigating the negative effects of aflatoxin B1 and deoxynivalenol. Gilts at 8.7 ± 0.5 kg body weight were allotted to four treatments: NC (uncontaminated diet); PC (contaminated diet: 150 µg aflatoxin B1 and 1100 µg deoxynivalenol per kg feed); HT (PC + humate, 0.5%); and EM (PC + β-mannanase, 800 U/kg diet). Growth performance was recorded for 42 days, and blood and tissue samples were collected for hematological and histopathological evaluations. The PC reduced (p < 0.05) serum tumor necrosis factor-α at day 28 and tended to increase (p = 0.062) immunoglobulin G (IgG), whereas the EM reduced IgG (p < 0.05) at day 42. The PC increased (p < 0.05) mean corpuscular hemoglobin and volume, which were reduced (p < 0.05) by HT or EM at day 42. The PC increased (p < 0.05) bile duct hyperplasia, which was attenuated (p < 0.05) by HT or EM. The PC reduced (p < 0.05) gain- to-feed ratio for the overall period, whereas HT increased (p < 0.05) average daily gain on days 21 to 28. These results suggest that HT and EM may mitigate mycotoxin-induced immune and hepatic damage in pigs through adsorbing mycotoxins. Full article
(This article belongs to the Special Issue Adverse Effects of Co-Contaminated Mycotoxins and Strategies for Their Mitigation)

Review

Jump to: Research

37 pages, 1571 KB  
Review
Biological Detoxification of Mycotoxins by Lactic Acid Bacteria: Safeguarding Food from Fungal Contaminants
by Nazia Tabassum, Minji Kim, Tae-Hee Kim, Du-Min Jo, Won-Kyo Jung, Young-Mog Kim and Fazlurrahman Khan
Toxins 2026, 18(5), 236; https://doi.org/10.3390/toxins18050236 - 20 May 2026
Abstract
Mycotoxins are one of the biggest threats to global food safety, public health, and economic stability. More than 400 mycotoxins have been found to be secondary metabolites of toxigenic fungi, mostly from the genera Aspergillus, Fusarium, Penicillium, and Alternaria. [...] Read more.
Mycotoxins are one of the biggest threats to global food safety, public health, and economic stability. More than 400 mycotoxins have been found to be secondary metabolites of toxigenic fungi, mostly from the genera Aspergillus, Fusarium, Penicillium, and Alternaria. Aflatoxins (AFs), ochratoxin A (OTA), deoxynivalenol (DON), zearalenone (ZEA), fumonisins (FBs), patulin (PAT), and T-2/HT-2 toxins are the most dangerous to the health of people and animals. Conventional physical and chemical decontamination methods are only partially effective and can reduce food quality, leave toxic residues, or be too expensive for smallholder food systems. Recent studies have shown that the application of lactic acid bacteria (LAB) as a biological detoxification method is a safe, cost-effective, and environmentally friendly option, and has a long history of safe use in fermented foods. Selected strains or taxonomic units have been granted GRAS status by the FDA or QPS (Qualified Presumption of Safety) status by EFSA. However, their use for mycotoxin detoxification still requires strain-level safety assessment and efficacy validation in the intended food matrix. There are several mechanisms by which LAB employ to reduce the bioavailability of mycotoxins in food systems: (i) physical adsorption via cell wall components such as peptidoglycan, teichoic acids, and exopolysaccharides; (ii) enzymatic biotransformation that may produce non-toxic or less-toxic metabolites, though the safety of degradation products requires case-by-case toxicological assessment; (iii) antifungal metabolite production that inhibits fungal growth and mycotoxin biosynthesis; and (iv) competitive exclusion of toxigenic fungi during fermentation. This comprehensive review examines the existing evidence on the detoxification of major food mycotoxins by LAB, with an emphasis on mechanisms, strain-specific efficacy, food-matrix applications, and factors that affect detoxification efficacy. Discussion has also been made of translating in vitro findings to in vivo settings and food-scale applications, alongside regulatory frameworks, current challenges, and future research directions. The review also suggests ways to combine LAB with new technologies, such as encapsulation, genetic engineering, and fermentation optimization, to make food systems safer by synergistically controlling mycotoxins. Full article
(This article belongs to the Special Issue Adverse Effects of Co-Contaminated Mycotoxins and Strategies for Their Mitigation)
28 pages, 531 KB  
Review
Multiple Mycotoxin Contamination in Livestock Feed: Implications for Animal Health, Productivity, and Food Safety
by Oluwakamisi F. Akinmoladun, Fabia N. Fon, Queenta Nji, Oluwaseun O. Adeniji, Emmanuel K. Tangni and Patrick B. Njobeh
Toxins 2025, 17(8), 365; https://doi.org/10.3390/toxins17080365 - 25 Jul 2025
Cited by 22 | Viewed by 6936
Abstract
Mycotoxins are toxic secondary metabolites produced by various fungi that contaminate livestock feed, posing serious threats to animal health, productivity, and food safety. Although historical research has often examined individual mycotoxins in isolation, real-world conditions typically involve the simultaneous presence of multiple mycotoxins, [...] Read more.
Mycotoxins are toxic secondary metabolites produced by various fungi that contaminate livestock feed, posing serious threats to animal health, productivity, and food safety. Although historical research has often examined individual mycotoxins in isolation, real-world conditions typically involve the simultaneous presence of multiple mycotoxins, resulting in additive or synergistic toxic effects that are often more severe than those observed with single toxin exposures. This review comprehensively synthesizes recent findings on multi-mycotoxin contamination in livestock feed, highlighting their physiological effects, mechanisms of action, and implications for regulatory frameworks. Multi-mycotoxin interactions exacerbate oxidative stress, immune suppression, impaired reproduction, and organ damage across species, leading to reduced growth performance, decreased milk and egg production, compromised carcass and wool quality, and increased mortality rates. A major concern is that current international regulatory standards mainly address individual mycotoxins, overlooking the compounded risks of co-occurrence. Global surveillance studies consistently reveal high prevalence rates of mycotoxin mixtures in feedstuffs, especially combinations involving DON, ZEN, AFB1, FB1, and OTA. Understanding these interactions and their underlying cellular mechanisms is critical for improving risk assessment models, formulating integrated mitigation strategies, and safeguarding both livestock productivity and human food security. Full article
(This article belongs to the Special Issue Adverse Effects of Co-Contaminated Mycotoxins and Strategies for Their Mitigation)
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