Pharmacological Intervention Against Toxicity of Environmental Pollutants and Stresses

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Human Toxicology and Epidemiology".

Deadline for manuscript submissions: 31 December 2025 | Viewed by 685

Special Issue Editors


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Guest Editor
Key Laboratory of Environmental Medicine Engineering of Ministry of Education, Medical School, Southeast University, Nanjing, China
Interests: environmental toxicology; nanotoxicology; microplastics; emerging contaminants; mechanism-specific toxicity; pharmacology
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Guest Editor
Institute of Biophysics and Biomedical Engineering, Bulgarian Academy of Sciences, Sofia, Bulgaria
Interests: nanotoxicology; pharmacology
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Guest Editor
School of Public Health, Southeast University, Nanjing, China
Interests: nanotoxicology; neurotoxicology; environment and health; nanoplastics

Special Issue Information

Dear Colleagues,

In the Special Issue “Pharmacological Intervention against Toxicity of Environmental Pollutants and Stresses”, we emphasize that our exclusive focus is on human health, addressing the pharmacological study and efficacy assessment of various drugs or chemicals that alleviate the toxic effects caused by environmental pollutants and stresses. We invite manuscripts that explore this critical area, with the scope including but not limited to the following: (1) Risk assessment and intervention of different environmental pollutants and stresses; (2) cellular and molecular mechanisms of pharmacological intervention;  (3) therapy on diseases relevant to environmental pollutants and stresses; (4) new methods or strategies of pharmacological intervention against toxicity of environmental pollutants and stresses. Recently, there has been a pressing need to mitigate the adverse health impacts of environmental pollutants (such as emergent contaminants) and stressors (such as heat stress) that are increasingly recognized as the global health threat. Therefore, this Special Issue aims to provide insights on effective strategies to protect and restore human health by exploring the potential of pharmacological agents to counteract the toxic effects of environmental pollutants and stresses.

Prof. Dr. Dayong Wang
Prof. Dr. Natalia Krasteva
Dr. Tianshu Wu
Guest Editors

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Keywords

  • toxicology
  • ecotoxicology
  • pharmacology
  • environmental pollutant
  • environmental stress
  • health protection

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Published Papers (1 paper)

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Research

14 pages, 1429 KiB  
Article
Long-Term Exposure to 6-PPD Quinone Inhibits Glutamate Synthesis and Glutamate Receptor Function Associated with Its Toxicity Induction in Caenorhabditis elegans
by Wei Wang, Yunhui Li and Dayong Wang
Toxics 2025, 13(6), 434; https://doi.org/10.3390/toxics13060434 - 26 May 2025
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Abstract
6-PPD quinone (6-PPDQ) is widely distributed in environments. In Caenorhabditis elegans, we first examined the effects of 6-PPDQ on glutamate synthesis and receptor function by analyzing glutamate content, related gene expression, and phenotypes after RNAi of these genes. Moreover, we performed glutamate [...] Read more.
6-PPD quinone (6-PPDQ) is widely distributed in environments. In Caenorhabditis elegans, we first examined the effects of 6-PPDQ on glutamate synthesis and receptor function by analyzing glutamate content, related gene expression, and phenotypes after RNAi of these genes. Moreover, we performed glutamate treatment after 6-PPDQ exposure to determine the potential pharmacological effects of glutamate against 6-PPDQ toxicity. After exposure, the glutamate content was reduced by 0.1–10 μg/L 6-PPDQ, which was due to decreased expression of W07E1.1, glna-1/2/3, and alh-6 governing glutamate synthesis from α-ketoglutarate, glutamine, and proline. RNAi of W07E1.1, glna-1/2/3, and alh-6 decreased glutamate content in 6-PPDQ-exposed nematodes, and caused susceptibility to 6-PPDQ toxicity. Among glutamate transporter genes, glt-1 expression was decreased by 0.1–10 μg/L 6-PPDQ. Moreover, 0.1–10 μg/L 6-PPDQ decreased glutamate receptor genes (glr-1, glr-2, and glr-4), and their expression was decreased by RNAi of W07E1.1, glna-1/2/3, alh-6, and glt-1. RNAi of these receptor genes resulted in susceptibility to 6-PPDQ toxicity, and daf-7, jnk-1, and dbl-1 were identified as targets of neuronal glr-1, glr-2, and glr-4. Furthermore, 5 mM glutamate suppressed 6-PPDQ toxicity and increased expression of glr-1, glr-2, and glr-4. Our results demonstrated the risk of 6-PPDQ exposure in disrupting glutamate synthesis and affecting function of glutamate receptors, which was related to 6-PPDQ toxicity induction. Full article
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