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Molecular Mechanisms of Pesticide Toxicity and Action

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: 20 July 2026 | Viewed by 682

Special Issue Editor


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Guest Editor
EHESP, Inserm, Irset (Institut de Recherche en Santé, Environnement et Travail), Université de Rennes, Campus Sante de Villejean—UMR_S 1085, F-35000 Rennes, France
Interests: epigenetics; animal reproduction; transcriptomics; next generation sequencing; gene expression and chromatin biology; recombination; RNA genetics; developmental biology; molecular biology

Special Issue Information

Dear Colleagues,

In modern agriculture, a huge array of pesticides is used to control pests, fungi, and undesirable plants. The negative effects of pesticides increase when pesticide actions are combined with other industrial pollutants, such as urban air,  perfluoroalkyl and polyfluoroalkyl substances, heavy metals, micotoxins, and plasticizers. The effects of pesticides are also enhanced due to global warming.

While several studies suggest that pesticides could impact many cellular processes, including neuroendocrine and endocrine functions, detoxification systems, the brain–gut microbiota axis, the brain, and reproductive organs, the mechanisms of toxicity at environmental low doses are still uncertain, as many studies have a tendency to use elevated doses. It is still not wholly understood whether the acquired effects could be long-lasting through epigenetic inheritance mechanisms that could impact an individual’s life over a long period after the exposure. We also need to reveal whether ancestral exposure could impact several generations. Additionally, sex-specific differences are still not well described. The discovery of new biomarkers of exposure and effects would be beneficial for human epidemiological studies.

In this Special Issue, manuscripts describing the mechanisms of pesticide toxicity are welcome. This could include the molecular mechanisms of pesticides using model organisms, as well as the human organoid models.

Dr. Fatima Smagulova
Guest Editor

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Keywords

  • neonicotinoids
  • sex-specific effects
  • brain–gut–microbiome
  • endocrine organs
  • genotoxic effects
  • epigenetic effects

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Published Papers (1 paper)

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Research

24 pages, 3145 KB  
Article
Intergenerational Effects of Neonicotinoid Thiacloprid in Murine Prostate Tissue Are Associated with Epigenetic Alterations in Homeobox Hox Genes
by Ouzna Dali, Shereen Cynthia D’Cruz, Chaima Diba Lahmidi, Tayeb Mohammed Belkhir, Theo De Gestas, Christine Kervarrec, Pierre-Yves Kernanec and Fatima Smagulova
Int. J. Mol. Sci. 2026, 27(7), 2921; https://doi.org/10.3390/ijms27072921 - 24 Mar 2026
Viewed by 458
Abstract
Neonicotinoids are widely used pesticides that have caused a catastrophic decrease in bee and bumblebee populations worldwide. In addition to insects, neonicotinoids induce toxic effects in other species, including lizards, birds, and mammals. Previous studies have shown that gestational exposure to thiacloprid promotes [...] Read more.
Neonicotinoids are widely used pesticides that have caused a catastrophic decrease in bee and bumblebee populations worldwide. In addition to insects, neonicotinoids induce toxic effects in other species, including lizards, birds, and mammals. Previous studies have shown that gestational exposure to thiacloprid promotes transgenerational effects in the testes and thyroid. In this project, we described the epigenetic effects of thiacloprid on prostate tissue in directly exposed F1 and non-directly exposed F3 outbred Swiss male mice. We used paraffin sections for morphological analysis and frozen tissue for immunofluorescence analysis, RT–qPCR, and protein analysis. We purified histones and analyzed them through Western blot. We used ChIP–qPCR for histone H3K4me3 occupancy analysis. A tendency to increase in epithelial hyperplasia in F1 but not in F3 prostate was detected. Elevated levels of phosphorylated histone H3 at serine 10, a marker of mitosis, in both the F1 and F3 prostates were noted. A significant increase in the level of the Ki-67 marker of proliferation was detected in the F1 but not in the F3 anterior prostate. Hox gene expression was upregulated in the F1 and downregulated in the F3 prostate. The changes in gene expression were positively associated with histone H3K4me3 alterations at the promoters of the Hoxa and Hoxb13 genes. We determined that regions of Hox genes that play important roles in prostate development had altered DNA methylation in the sperm of F1 and F3. These alterations in DNA methylation were negatively related to gene expression. This is an observational study, as it was part of our previous research on the effects of thiacloprid on the testis and thyroid. Our analysis revealed that gestational exposure to thiacloprid induced an increase in cell proliferation in the prostates of directly exposed F1. Some persistent epigenetic alterations in the prostate of F3 males were not associated with phenotypic changes. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Pesticide Toxicity and Action)
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