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Toxics
Special Issues
Toxicity and Molecular Mechanisms of Environmental Contaminants on Animals
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Toxicity and Molecular Mechanisms of Environmental Contaminants on Animals

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Novel Methods in Toxicology Research".

Deadline for manuscript submissions: 15 January 2026 | Viewed by 1020

Special Issue Editors

Prof. Dr. Chunmei Li

E-Mail Website
Guest Editor
College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China
Interests: environmental pollution; livestock environment and health; toxics; feed toxicolgoy
Special Issues, Collections and Topics in MDPI journals
Dr. Dan Shen

E-Mail Website
Guest Editor Assistant
College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China
Interests: air pollutants; respirotary injury; animal house environment; animal health; toxics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The growing prevalence of environmental contaminants significantly threatens animal health and ecological balance, highlighting the need to understand their toxicity and molecular mechanisms. Pollutants such as particulate matter, heavy metals, pesticides, microplastics, and emerging chemicals infiltrate animal systems via air, water, and food, disrupting physiological and cellular processes. Investigating these effects not only enhances our comprehension of contaminant impact, but also informs the development of effective strategies for ecological conservation and public health protection.

This Special Issue, “Toxicity and Molecular Mechanisms of Environmental Contaminants on Animals”, invites research on the biochemical pathways altered by these contaminants, their bioaccumulation, and cascading effects on animal behavior and health. Submissions focusing on advanced technologies like transcriptomics and metabolomics, or topics such as toxicant bioaccumulation, epigenetic roles, synergistic effects, and conservation implications, are encouraged. Contributions will enrich scientific understanding and foster innovative solutions to mitigate the impact of environmental contaminants.

Prof. Dr. Chunmei Li
Guest Editor

Dr. Dan Shen
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 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 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. Toxics 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 2600 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

  • environmental toxicants
  • animal health
  • molecular pathways
  • bioaccumulation
  • toxic injury

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

15 pages, 2473 KiB  
Article
Selenium Reduces Cadmium-Induced Cardiotoxicity by Modulating Oxidative Stress and the ROS/PARP-1/TRPM2 Signalling Pathway in Rats
by Yener Yazğan, Ömer Faruk Keleş, Mehmet Hafit Bayir, Hacı Ahmet Çiçek, Adem Ahlatcı and Kenan Yıldızhan
Toxics 2025, 13(8), 611; https://doi.org/10.3390/toxics13080611 - 22 Jul 2025
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Abstract
Cadmium (CAD) is a prevalent environmental contaminant that poses serious cardiotoxic risks. The heart, kidney, liver, and brain are just a few of the essential organs that can sustain serious harm from CAD, a very poisonous heavy metal. The cardiotoxic mechanism of CAD [...] Read more.
Cadmium (CAD) is a prevalent environmental contaminant that poses serious cardiotoxic risks. The heart, kidney, liver, and brain are just a few of the essential organs that can sustain serious harm from CAD, a very poisonous heavy metal. The cardiotoxic mechanism of CAD is linked to oxidative damage and inflammation. A trace element with anti-inflammatory, anti-apoptotic, and antioxidant qualities, selenium (SEL) can be taken as a dietary supplement. The biotoxicity of heavy metal CAD is significantly inhibited by SEL, a mineral that is vital to human and animal nutrition. Through ROS-induced PARP-1/ADPR/TRPM2 pathways, this study seeks to assess the preventive benefits of selenium against cardiovascular damage caused by CAD. The SEL showed encouraging results in reducing inflammatory and oxidative reactions. Rats were given 0.5 mg/kg SEL and 3 mg/kg 2-Aminoethyl diphenylborinate (2-APB) intraperitoneally for five days, in addition to 25 mg/kg CAD given via gavage. Histopathological examination findings revealed that the morphologic changes in the hearts of the CAD group rats were characterised by marked necrosis and the degeneration of myocytes and congestion of vessels. Compared to the rats in the CAD group, the hearts of the SEL, 2-APB and SEL+2-APB groups showed fewer morphological alterations. Moreover, in rats given CAD, there was an increase in cardiac malondialdehyde (MDA), total oxidant (TOS), reactive oxygen species (ROS), caspase (Casp-3-9), and TNF-α, whereas glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and total antioxidant (TAS) decreased. SEL improved antioxidants, avoided tissue damage, and reduced cardiac MDA, TOS, and ROS. In rats given CAD, SEL decreased cardiac PARP-1, TRPM2, TNF-α, and caspase. In summary, by reducing oxidative stress and cardiac damage and modifying the ROS/PARP-1/TRPM2 pathway, SEL protected against CAD cardiotoxicity. Full article
(This article belongs to the Special Issue Toxicity and Molecular Mechanisms of Environmental Contaminants on Animals)
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15 pages, 2682 KiB  
Article
Effects of Diethylstilbestrol on the Structure and Function of the Spleen in Male Golden Hamsters
by Jian Li, Ruiping Xu, Qingwei Wang, Xue Bai, Yanhua Su, Yaoxing Chen and Jing Cao
Toxics 2025, 13(5), 397; https://doi.org/10.3390/toxics13050397 - 15 May 2025
Viewed by 528
Abstract
With industrial development, endocrine-disrupting chemicals have continued to accumulate in the environment, attracting growing attention due to their potential effects on biological health. The reproductive toxicity of diethylstilbestrol (DES), a synthetic estrogen widely present in the environment, is widely documented; however, studies on [...] Read more.
With industrial development, endocrine-disrupting chemicals have continued to accumulate in the environment, attracting growing attention due to their potential effects on biological health. The reproductive toxicity of diethylstilbestrol (DES), a synthetic estrogen widely present in the environment, is widely documented; however, studies on its effects on the immune system remain limited. In this study, adult male golden hamsters were subcutaneously administered varying doses of DES (0, 0.01, 0.1, and 1.0 mg/kg) for seven consecutive days to assess its immunomodulatory impact on peripheral blood and the spleen. We found that the DES treatment significantly reduced spleen index, white pulp area, and splenic lymphocyte proliferation while increasing caspase-3-positive apoptotic cells and inducible nitric oxide synthase expression. In peripheral blood, DES induced a dose-dependent suppression of lymphocyte proliferation, with lipopolysaccharide- and concanavalin A-stimulated proliferation reduced by 47.68–71.76% and 44.23–72.7%, respectively. Concurrently, DES significantly downregulated the pro-inflammatory cytokines IL-2 and IFN-γ (p < 0.01) while upregulating the anti-inflammatory cytokines IL-4 and IL-10 (p < 0.01). Furthermore, DES treatment impaired antioxidant defenses, decreasing the activity of superoxide dismutase, glutathione peroxidase, and catalase while elevating malondialdehyde levels. Notably, DES led to the upregulation of G protein-coupled estrogen receptor and estrogen receptor α at both transcriptional and protein levels, whereas estrogen receptor β mRNA expression increased despite a decline in protein levels. This study provides critical experimental evidence elucidating the immunoregulatory effects of endocrine-disrupting environmental estrogens. Full article
(This article belongs to the Special Issue Toxicity and Molecular Mechanisms of Environmental Contaminants on Animals)
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