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Toxins
Special Issues
Plant Toxin Emergency
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Plant Toxin Emergency

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

Deadline for manuscript submissions: 30 June 2025 | Viewed by 1392

Special Issue Editors

Prof. Dr. Andrea Bolognesi

E-Mail Website
Guest Editor
Department of Medical and Surgical Sciences-DIMEC, General Pathology Section, Alma Mater Studiorum University of Bologna, 40126 Bologna, Italy
Interests: Xanthine oxidoreductase; oxidative stress; uric acid; nitric oxide; cytotoxicity; plant toxin; rRNA glycosylase; immunotoxin; targeted therapy; anti-tumour therapy
Special Issues, Collections and Topics in MDPI journals
Dr. Massimo Bortolotti

E-Mail Website
Guest Editor
Department of Experimental, Diagnostic and Specialty Medicine-DIMES, General Pathology Section, Alma Mater Studiorum—University of Bologna, Via S. Giacomo 14, 40126 Bologna, Italy
Interests: cell death; immunoconjugates; immunotherapy; immunotoxins; lectins; oxidative stress; plant toxins; ribosome-inactivating proteins; ricin; xanthine oxidoreductase
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Plant toxins are natural compounds that are found in several plant species and act as a defense mechanism against herbivores, pathogens and environmental stressors. Some common plant toxins include alkaloids, glycosides, terpenoids, and protein molecules, including ribosome-inactivating proteins and various lectins. Some of these toxins can be highly toxic and thus capable of causing serious health problems in animals and humans. While many plant toxins pose health risks, some are used medicinally for therapeutic purposes. However, the improper handling or ingestion of these toxins can lead to symptoms ranging from nausea and vomiting to organ failure and death. Possessing a comprehensive understanding of plant toxins is fundamental in fields such as toxicology, agriculture and medicine; this is in order to mitigate risks and exploit their potential benefits safely.

This Special Issue focuses on the growing public health concern related to plant toxins. This Special Issue welcomes the submission of research, case reports and clinical insights that highlight the importance of understanding, preventing and treating plant toxin exposures.

Key themes include:

  1. The identification and distribution of toxic plant species. Highlighting common and lesser-known toxic plants in different regions, and emphasizing the need for accurate identification and public awareness to prevent accidental exposures.
  2. Mechanisms of toxicity. Exploring the pathogenic mechanisms and biochemical pathways of intoxication, detailing how plant toxins can interfere with physiological functions and the resulting clinical manifestations.
  3. Clinical management and treatment protocols. Presenting updated protocols for the management of plant toxin-related emergencies, from initial diagnosis to advanced treatments such as antidotes, supportive care and novel therapeutic approaches.
  4. Public health and safety. Providing an overview of small toxic molecules (alkaloids, glycosides, glucosinolates and others) and plant protein toxins, especially ribosome-inactivating proteins and toxic lectins, that can pose serious public health risks if consumed or handled improperly. Public health and safety concerns involve preventing accidental ingestion, handling these substances with caution, and raising awareness about their risks, particularly in bioterrorism or after accidental exposure.
  5. Case studies. Featuring real-life cases of plant toxin exposure, offering practical insights into diagnosis, management challenges and outcomes. These case studies provide valuable lessons for healthcare professionals and first responders.

This Special Issue aims to proviede a comprehensive understanding of the challenges and strategies associated with plant toxin emergencies. By advancing knowledge in this area, this Special Issue also aims to enhance response efforts and ultimately reduce the impact of plant toxins on human health.

Prof. Dr. Andrea Bolognesi
Dr. Massimo Bortolotti
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

  • plant toxins
  • secondary metabolites
  • alkaloids
  • ribosome-inactivating proteins
  • toxic lectins
  • biological activity
  • toxicity mechanisms
  • clinical features of intoxication
  • bioterrorism
  • toxin detection

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Published Papers (2 papers)

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Research

14 pages, 2964 KiB  
Article
The Secretome of Brain Endothelial Cells Exposed to the Pyrrolizidine Alkaloid Monocrotaline Induces Astrocyte Reactivity and Is Neurotoxic
by Letícia Oliveira Santos, Julita Maria Pereira Borges, Juliana Lago Leite, Mauricio Moraes Victor, Adriana Lopes da Silva, Cleonice Creusa dos Santos, Victor Diógenes Amaral da Silva, Ravena Pereira do Nascimento and Silvia Lima Costa
Toxins 2025, 17(2), 65; https://doi.org/10.3390/toxins17020065 (registering DOI) - 1 Feb 2025
Viewed by 330
Abstract
Monocrotaline (MCT) has well-characterized hepatotoxic and pneumotoxic effects attributed to its active pyrrole metabolites. Studies have previously shown that astrocytes and neurons are targets of MCT, and that toxicity is attributed to astrocyte P450 metabolism to reactive metabolites. However, little is known about [...] Read more.
Monocrotaline (MCT) has well-characterized hepatotoxic and pneumotoxic effects attributed to its active pyrrole metabolites. Studies have previously shown that astrocytes and neurons are targets of MCT, and that toxicity is attributed to astrocyte P450 metabolism to reactive metabolites. However, little is known about MCT toxicity and metabolism by brain endothelial cells (BECs), cells that, together with astrocytes, are specialized in xenobiotic metabolism and neuroprotection. Therefore, in the present study, we evaluated the toxicity of MCT in BECs, and the effects on astrocyte reactivity and neuronal viability in vitro. MCT was purified from Crotalaria retusa seeds. BECs, obtained from the brain of adult Wistar rats, were treated with MCT (1–500 µM), and cell viability and morphology were analyzed after 24–72 h of treatment. Astrocyte/neuron co-cultures were prepared from the cortex of neonatal and embryonic Wistar rats, and the cultures were exposed to conditioned medium (secretome) derived from BECs previously treated with MCT (100–500 µM, SBECM100/500). MCT was not toxic to BECs at the concentrations used and induced a concentration-dependent increase in cell dehydrogenase after 72 h of treatment, suggesting resistance to damage and drug metabolism. However, exposure of astrocyte/neuron co-cultures to the SBECM for 24 h induced changes in the cell morphology, vacuolization, and overexpression of GFAP in astrocytes, characterizing astrogliosis, and neurotoxicity with a reduction in the length of neurites labeled for β-III-tubulin, effects that were MCT concentration-dependent. These results support the hypothesis that MCT neurotoxicity may be due to products of its metabolism by components of the BBB such as BECs and astrocytes, which may be responsible for the brain lesions and symptoms observed after intoxication. Full article
(This article belongs to the Special Issue Plant Toxin Emergency)
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16 pages, 14718 KiB  
Article
Repair of Retrorsine-Induced DNA Damage in Rat Livers: Insights Gained from Transcriptomic and Proteomic Studies
by Yun Long, Yiwei Wang, Zijing Song, Xin He, Yisheng He and Ge Lin
Toxins 2024, 16(12), 538; https://doi.org/10.3390/toxins16120538 - 13 Dec 2024
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Abstract
Pyrrolizidine alkaloids (PAs) are common phytotoxins that are found worldwide. Upon hepatic metabolic activation, the reactive PA metabolites covalently bind to DNAs and form DNA adducts, causing mutagenicity and tumorigenicity in the liver. However, the molecular basis of the formation and removal of [...] Read more.
Pyrrolizidine alkaloids (PAs) are common phytotoxins that are found worldwide. Upon hepatic metabolic activation, the reactive PA metabolites covalently bind to DNAs and form DNA adducts, causing mutagenicity and tumorigenicity in the liver. However, the molecular basis of the formation and removal of PA-derived DNA adducts remains largely unexplored. In the present study, Sprague Dawley (SD) rats were exposed to retrorsine (RTS), a representative PA, at a human-relevant dose of 3.3 mg/kg/day for 28 days. The rats were divided into three groups: control, RTS-28 (sacrificed after continuous RTS exposure), and RTS-161 (sacrificed at 133 days post-RTS-exposure). The multi-omics analyses demonstrated the involvement of homologous recombination (HR) and non-homologous end joining (NHEJ) repair pathways as a response to PA-induced DNA damage. Additionally, the characteristic guanine adducts induced by RTS exposure were in accordance with the higher expression of XPA and XPC, indicating that nucleotide excision repair (NER) and base excision repair (BER) also contributed to repairing RTS-induced DNA damage. Furthermore, we also showed that DNA damage persisted after PA exposure, and mutagenically related repair errors might occur due to the prolonged genotoxic effects. The present study lays the foundation for bridging PA-derived DNA adducts, DNA damage, DNA repair, and the follow-up mutagenesis and carcinogenesis associated with PA exposure. Full article
(This article belongs to the Special Issue Plant Toxin Emergency)
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