Toxicological Studies Using Zebrafish Models

A special issue of Toxics (ISSN 2305-6304).

Deadline for manuscript submissions: 31 July 2025 | Viewed by 811

Special Issue Editors


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Guest Editor
Centre of Marine Sciences (CCMAR), Faculty of Medicine and Biomedical Sciences in University of Algarve, Portugal and GreenColab, 8005-139 Faro, Portugal
Interests: zebrafish; fish skeletal malformations
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Guest Editor
College of Animal Science and Technology, Inner Mongolia Minzu University, Tongliao 028000, China
Interests: traditional Chinese medicine; ethnic medicine; environmental pollutants; safety assessment; zebrafish disease models

Special Issue Information

Dear Colleagues,

Zebrafish are crucial models in toxicology, particularly in disease modeling. Frequently used in drug screening, including in safety evaluations of synthetic drugs, traditional Chinese medicine, and ethnic medicine, they are fast, sensitive, and cost-effective, making them highly valuable for the initial high-throughput screening of drug (toxicant) effects.

In the realm of environmental toxicology, zebrafish play a vital role in monitoring the levels of various harmful substances that impact human health. These substances include persistent organic pollutants, pesticides, and heavy metals, among others. The genetic similarity between zebrafish and humans makes zebrafish effective for simulating human responses to both drugs and environmental pollutants; as such, they are an indispensable tool in toxicological studies.

This Special Issue aims to collect a broad spectrum of novel research in the field of toxicology, using zebrafish as the model organism. We look forward to receiving your contributions.

Dr. Paulo Jorge Gavaia
Prof. Dr. Dong Wu
Guest Editors

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Keywords

  • zebrafish model
  • toxic substance
  • drugs
  • safety assessment
  • molecular mechanisms

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Published Papers (2 papers)

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Research

14 pages, 1228 KiB  
Article
N-Acetylcysteine-Amide Protects Against Acute Acrylamide Neurotoxicity in Adult Zebrafish
by Niki Tagkalidou, Júlia Goyenechea-Cunillera, Irene Romero-Alfano, Maria Olivella Martí, Juliette Bedrossiantz, Eva Prats, Cristian Gomez-Canela and Demetrio Raldúa
Toxics 2025, 13(5), 362; https://doi.org/10.3390/toxics13050362 (registering DOI) - 30 Apr 2025
Abstract
Acrylamide (ACR) is a potent neurotoxicant that disrupts cellular redox homeostasis by depleting reduced glutathione (GSH) and inducing oxidative stress. Despite its well-characterized mechanism, no effective treatments for ACR-induced neurotoxicity currently exist. This study evaluates the therapeutic efficacy of N-acetylcysteine-amide (AD4), a blood–brain [...] Read more.
Acrylamide (ACR) is a potent neurotoxicant that disrupts cellular redox homeostasis by depleting reduced glutathione (GSH) and inducing oxidative stress. Despite its well-characterized mechanism, no effective treatments for ACR-induced neurotoxicity currently exist. This study evaluates the therapeutic efficacy of N-acetylcysteine-amide (AD4), a blood–brain barrier (BBB)-permeable derivative of N-acetylcysteine, in a novel severe acute ACR neurotoxicity model in adult zebrafish. Adult zebrafish received a single intraperitoneal (i.p.) injection of ACR (800 μg/g), followed by AD4 (400 μg/g i.p.) or PBS 24 h later. ACR exposure reduced brain GSH levels by 51% reduction at 48 h, an effect fully reversed by AD4 treatment. Behavioral analyses showed that AD4 rescued ACR-induced deficits in short-term habituation of the acoustic startle response (ASR). Surprisingly, ACR exposure did not alter the neurochemical profile of key neurotransmitters or the expression of genes related to redox homeostasis, synaptic vesicle recycling, regeneration, or myelination. These results demonstrate AD4’s neuroprotective effects against acute ACR-induced brain toxicity, highlighting its therapeutic potential and validating adult zebrafish as a translational model for studying neurotoxic mechanisms and neuroprotective interventions. Full article
(This article belongs to the Special Issue Toxicological Studies Using Zebrafish Models)
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16 pages, 3724 KiB  
Article
The Neurobehavioral Impact of Zinc Chloride Exposure in Zebrafish: Evaluating Cognitive Deficits and Probiotic Modulation
by Madalina Ene, Alexandra Savuca, Alin-Stelian Ciobica, Roxana Jijie, Irina Luciana Gurzu, Luminita Diana Hritcu, Ionut-Alexandru Chelaru, Gabriel-Ionut Plavan, Mircea Nicusor Nicoara and Bogdan Gurzu
Toxics 2025, 13(3), 193; https://doi.org/10.3390/toxics13030193 - 8 Mar 2025
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Abstract
Zinc contamination in aquatic environments has become a growing concern due to its potential to bioaccumulate and induce neurotoxic effects in aquatic organisms. As an essential trace element, zinc plays a crucial role in various physiological processes, but excessive exposure can disrupt the [...] Read more.
Zinc contamination in aquatic environments has become a growing concern due to its potential to bioaccumulate and induce neurotoxic effects in aquatic organisms. As an essential trace element, zinc plays a crucial role in various physiological processes, but excessive exposure can disrupt the gut–brain axis, leading to cognitive and behavioral impairments. Recent studies have suggested that probiotics may offer protective effects against environmental neurotoxins by modulating the gut microbiota and associated neurological functions. The zebrafish (Danio rerio) has emerged as a valuable model organism for studying the biological mechanisms underlying neurotoxicity and potential therapeutic interventions. This study aimed to assess the effects of probiotics on cognitive impairments induced by zinc chloride (ZnCl2) exposure in zebrafish. Specifically, zebrafish were exposed to ZnCl2 at concentrations of 0.5 mg/L and 1.0 mg/L for 96 h, followed by a 7-day post-exposure period to probiotics (Bifidobacterium longum, Bifidobacterium animalis lactis, Lactobacillus rhamnosus). ZnCl2 exposure at these concentrations is already known to induce behavioral and neuromotor deficits resembling Alzheimer’s disease-like symptoms in zebrafish models, making it a suitable model for evaluating the neuroprotective potential of probiotics. Behavioral assessments including sociability tests along with short- and long-term memory evaluations were conducted using EthoVision XT 16 software. Memory tests demonstrated that ZnCl2 exposure impaired cognitive functions, while probiotic treatment did not significantly ameliorate these deficits. In the social behavior test, ZnCl2 at 0.5 mg/L resulted in a marked decrease in sociability, whereas exposure to 1.0 mg/L did not induce significant changes. However, post-exposure probiotic administration following ZnCl2 intoxication at 1.0 mg/L exhibited an anxiolytic effect on zebrafish. These findings suggest that probiotics may exhibit partial neurobehavioral benefits following zinc chloride-induced toxicity, particularly in mitigating anxiety-like behaviors rather than cognitive deficits. Further investigations are needed to elucidate the precise mechanisms by which probiotics interact with the gut–brain axis in the context of heavy metal neurotoxicity. Full article
(This article belongs to the Special Issue Toxicological Studies Using Zebrafish Models)
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