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Toxins
Special Issues
Molecular Response of Hosts to Fungal Toxins
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Molecular Response of Hosts to Fungal Toxins

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

Deadline for manuscript submissions: 30 April 2026 | Viewed by 243

Special Issue Editors

Dr. Shaukat Ali

E-Mail Website
Guest Editor
Engineering Research Center of Biological Control, Ministry of Education and Guangdong Province, South China Agricultural University, Guangzhou 510642, China
Interests: biological control; biopesticides; entomopathogenic fungi; fungal toxins; agricultural pests; bio-safety of natural enemies
Dr. Jianhui Wu

E-Mail Website
Guest Editor
Engineering Research Center of Biological Control, Ministry of Education and Guangdong Province, South China Agricultural University, Guangzhou 510642, China
Interests: biological control; biopesticides; entomopathogenic fungi; fungal toxins; thrips

Special Issue Information

Dear Colleagues,

This Special Issue aims to explore the intricate molecular responses of host organisms to fungal toxins, shedding light on the biochemical pathways and genetic adaptations that mediate these interactions. Fungal toxins, or mycotoxins, pose significant threats to agricultural productivity and human health. Understanding the host's response at the molecular level is crucial for developing effective strategies to mitigate these risks. We invite contributions that encompass various aspects of host-fungal interactions, including but not limited to gene expression changes, signal transduction pathways, immune responses, and metabolic adaptations. By integrating findings from diverse fields such as molecular biology, toxicology, and plant pathology, this Special Issue will provide comprehensive insights into the dynamic interplay between hosts and fungal toxins.

Dr. Shaukat Ali
Dr. Jianhui Wu
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
  • host response
  • molecular biology
  • immune response
  • metabolic adaptation

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Published Papers (1 paper)

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Research

19 pages, 2298 KiB  
Article
The Emerging Mycotoxin 2-Amino-14, 16-Dimethyloctadecan-3-ol (AOD) Alters Transcriptional Regulation and Sphingolipid Metabolism and Undergoes N-Acylation by HepG2 Cells
by Shenlong Mo, Zhenying Hu, Huaiyi Zhu, Boming Yu, Xiaoyan Chen, Yu Chen, Alfred H. Merrill, Jr. and Jingjing Duan
Toxins 2025, 17(8), 413; https://doi.org/10.3390/toxins17080413 - 15 Aug 2025
Abstract
2-Amino-14,16-dimethyloctadecan-3-ol (AOD) is commonly found in foods contaminated with Fusarium avenaceum, particularly cereals or fruits, and is structurally related to Fusarium mycotoxins (fumonisins) and mammalian sphingoid bases, especially 1-deoxysphinganine (m18:0); therefore, it might enter systemic circulation and tissues upon dietary intake. Knowledge about [...] Read more.
2-Amino-14,16-dimethyloctadecan-3-ol (AOD) is commonly found in foods contaminated with Fusarium avenaceum, particularly cereals or fruits, and is structurally related to Fusarium mycotoxins (fumonisins) and mammalian sphingoid bases, especially 1-deoxysphinganine (m18:0); therefore, it might enter systemic circulation and tissues upon dietary intake. Knowledge about what happens when cells are exposed to AOD is limited, but it has been reported to be cytotoxic and to induce vacuolization in HepG2 cells. We also found that AOD is cytotoxic for HepG2 cells, but even at a concentration where cell viability remained above 85% (5 μM), it altered 24 differentially expressed genes based on RNA sequencing-based transcriptomic profiling. Among these genes, 13 were shared with cells treated with m18:0. These overlapping differentially expressed genes were primarily enriched in activated stress response pathways of cells, including the upregulation of specific genes in the hypoxia-inducible factor 1α (HIF-1α) signaling pathway, such as hexokinase 1 (HK1) and egl-9 family hypoxia-inducible factor 3 (EGLN3), the activation of key components in the p53 signaling pathway, and the induction of cellular senescence-associated transcriptional programs involving serpin family E member 1 (SERPINE1). Transcriptional analysis of genes related to sphingolipid metabolism showed that treatment with AOD increased the mRNA expression of ceramide synthase 4 (CerS4), sphingosine-1-phosphate phosphatase 1 (SGPP1), and UDP-glucosylceramide glucosyltransferase (UGCG), while decreasing the expression of dihydroceramide desaturase 1 (DEGS1) and fatty acid desaturase 3 (FADS3), a pattern of gene expression changes that mirrored the alterations observed with m18:0 treatment. Lipidomic analyses revealed that AOD significantly perturbed the sphingolipid composition of HepG2 cells, specifically increasing hexosylceramide content while decreasing ceramide and sphingomyelin levels. Moreover, AOD was found to undergo intracellular metabolism to N-acyl-AODs, perhaps by ceramide synthase(s), since this acylation was inhibited by fumonisin B1 (FB1). These findings demonstrate that AOD or possibly its N-acyl metabolites can alter cellular sphingolipid metabolism and affect the expression of genes involved in cell stress. These new insights call for more studies of the impact of this food contaminant on cells and the implications for human health. Full article
(This article belongs to the Special Issue Molecular Response of Hosts to Fungal Toxins)
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