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12.4
6.6
Journals
Antioxidants
Special Issues
Natural Antioxidants in Counteracting Mycotoxin and Heavy Metal Toxicity
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Natural Antioxidants in Counteracting Mycotoxin and Heavy Metal Toxicity

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: 31 July 2026 | Viewed by 1874

Special Issue Editors

Prof. Dr. Shusheng Tang

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: oxidative stress; molecular mechanism; toxicology; risk assessment; neurotoxicity
Special Issues, Collections and Topics in MDPI journals
Dr. Xingyao Pei

E-Mail Website
Guest Editor Assistant
Tianjin Key Laboratory of Agricultural Animal Breeding and Healthy Husbandry, College of Animal Science and Veterinary Medicine, Tianjin Agricultural University, Tianjin, China
Interests: animal nutrition

Special Issue Information

Dear Colleagues,

Mycotoxins and heavy metals are pervasive environmental contaminants, posing significant global threats to human and animal health through food chain contamination and environmental exposure. Their toxicity mechanisms, particularly the induction of oxidative stress, are major contributors to cellular damage, organ dysfunction, and chronic diseases. Natural antioxidants, including plant-derived polyphenols, flavonoids, terpenoids, vitamins, and microbial metabolites, offer immense potential in mitigating these toxic effects. These compounds often function through potent antioxidant activities, directly scavenging reactive oxygen species and enhancing endogenous antioxidant defenses. This Special Issue aims to compile cutting-edge research and reviews exploring the protective roles and mechanisms of natural antioxidants against key mycotoxins (aflatoxin, ochratoxin, deoxynivalenol, zearalenone, fumonisin) and heavy metals (lead, cadmium, arsenic, mercury). We welcome original research articles and comprehensive reviews investigating the detoxification potential, molecular mechanisms, in vitro and in vivo efficacy, and potential applications of these natural antioxidants in food safety, nutrition, and preventive medicine.

Prof. Dr. Shusheng Tang
Guest Editor

Dr. Xingyao Pei
Guest Editor Assistant

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 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. Antioxidants 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 2900 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

  • natural antioxidants
  • mycotoxins
  • heavy metal
  • detoxification

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Published Papers (2 papers)

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Research

22 pages, 10520 KB  
Article
Lycopene Protects Deoxynivalenol-Induced Intestinal Barrier Dysfunction and NLRP3 Inflammasome Activation by Targeting the ERK Pathway
by Zihui Cai, Zhi Lu, Youshuang Wang, Wenxi Song, Xu Yang and Cong Zhang
Antioxidants 2025, 14(12), 1513; https://doi.org/10.3390/antiox14121513 - 17 Dec 2025
Viewed by 513
Abstract
In agricultural production, Deoxynivalenol (DON) generally exists and contaminates wheat, corn, and other grains, causing intestinal damage and immunotoxicity. Lycopene (LYC), an antioxidant, anti-inflammatory carotenoid, is mainly found in red fruits such as tomatoes and has been investigated for its great medicinal advantages. [...] Read more.
In agricultural production, Deoxynivalenol (DON) generally exists and contaminates wheat, corn, and other grains, causing intestinal damage and immunotoxicity. Lycopene (LYC), an antioxidant, anti-inflammatory carotenoid, is mainly found in red fruits such as tomatoes and has been investigated for its great medicinal advantages. This study aimed to investigate the protective effect of LYC against DON-induced enterotoxicity. Our findings demonstrated that incubation of IPEC-J2 cells with 0.5 μM DON for 24 h caused intestinal barrier impairment and oxidative stress induction, which subsequently led to increased secretion of pro-inflammatory factors (TNF-α, IL-1β, IL-18, and IL-6) and decreased secretion of the counterregulatory factor (IL-10). Furthermore, DON ultimately induced NLRP3 inflammasome activation through the stimulation of the MAPK/NF-κB pathway. It is worth mentioning that the above changes were reversed after adding 30 μg/mL of LYC to DON-exposed IPEC-J2 cells. In addition, further experiments confirmed that ERK activator (4-Methylbenzylidene camphor, 4-MBC) eliminated the positive effect of LYC on alleviating enterotoxicity induced by DON in IPEC-J2 cells. In addition, further experiments confirmed that 4-MBC eliminated the positive effect of LYC on alleviating enterotoxicity induced by DON. In general, our study certified that ERK is a therapeutic target for LYC protecting DON-induced intestinal barrier dysfunction and NLRP3 inflammasome activation. Full article
(This article belongs to the Special Issue Natural Antioxidants in Counteracting Mycotoxin and Heavy Metal Toxicity)
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22 pages, 5118 KB  
Article
Investigating Nickel-Induced Neurotoxicity: Associations with Gut Microbiota Dysbiosis and Ferroptosis
by Yao Shen, Kai Cao, Wenjuan Zhang, Chun Chen, Chang Gao, Jingran Wang, Tian Xin, Cun Li, Shusheng Tang, Xingyao Pei and Daowen Li
Antioxidants 2025, 14(12), 1478; https://doi.org/10.3390/antiox14121478 - 9 Dec 2025
Viewed by 693
Abstract
Nickel is a pervasive heavy metal with the potential for multi-route exposure, raising significant concerns regarding systemic toxicity. Although Ni2+ has been implicated in nickel sulfate NiSO4-induced neurotoxicity, its underlying mechanisms remain incompletely elucidated. The present study investigates the role [...] Read more.
Nickel is a pervasive heavy metal with the potential for multi-route exposure, raising significant concerns regarding systemic toxicity. Although Ni2+ has been implicated in nickel sulfate NiSO4-induced neurotoxicity, its underlying mechanisms remain incompletely elucidated. The present study investigates the role of NiSO4-induced ferroptosis as a potential contributor to neurotoxicity. C57BL/6 mice were administered NiSO4 daily via oral gavage at doses of 50, 100, and 200 mg/kg over 28 days. Neurobehavioral assessments, histopathological examination, transmission electron microscopy, and molecular profiling were conducted to evaluate brain injury and ferroptotic activity. Gut microbiota composition and intestinal barrier integrity were systematically evaluated. In vitro, HT22 cells were subjected to NiSO4 treatment, followed by integrative transcriptomic analysis complemented by pharmacological and genetic manipulation to delineate the contributions of ferroptosis and autophagy. The results demonstrated that NiSO4 exposure inhibited body weight gain, elicited depression-like behaviors, and initiated ferroptosis, evidenced by ultrastructural mitochondrial damage and dysregulated expression of glutathione peroxidase 4/acyl-CoA synthetase long chain family member 4 (GPX4/ACSL4). Furthermore, NiSO4 caused gut microbiota dysbiosis and compromised the intestinal barrier, which was correlated with the induction of ferroptosis in neuronal cells of the brain. In HT22 cells, NiSO4 elicited dose-dependent cytotoxicity and lactate dehydrogenase (LDH) release. KEGG pathway enrichment analysis further revealed that NiSO4 treatment significantly upregulated pathways associated with ferroptosis, autophagy, and lysosomal function. Moreover, both ferrostatin-1 and rapamycin attenuated NiSO4-induced cytotoxicity and ferroptosis, indicating that autophagy serves a protective function against ferroptotic cell death. Additionally, overexpression of Transcription Factor EB (TFEB) attenuated NiSO4-induced ferroptosis by downregulating ACSL4, and upregulating GPX4, implicating the autophagy–lysosome pathway in the protective regulation of this cell death process. In summary, our findings indicated that NiSO4-induced neurotoxicity was strongly associated with gut microbiota dysbiosis and coincided with ferroptosis in the brain, while stimulation of the autophagy–lysosome pathway conferred neuroprotective effects via modulating TFEB-dependent anti-ferroptotic mechanisms. These findings offer novel insights for risk assessment and therapeutic strategies of nickel-related neurotoxicity. Full article
(This article belongs to the Special Issue Natural Antioxidants in Counteracting Mycotoxin and Heavy Metal Toxicity)
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