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Published on: April 28, 2023
Epigenetic Effects Promoted by Neonicotinoid Thiacloprid Exposure
Colin Hartman1, Louis Legoff1, Martina Capriati1
1EHESP, Inserm, Institut de Recherche en Santé, Environnement et Travail - UMR_S 1085, Université de Rennes 1, Rennes, France.
Gestational exposure to thiacloprid (thia) insecticide in mice reduced sperm count and caused telomere defects. This neonicotinoid exposure disrupts male reproductive health by affecting epigenetic regulation of meiosis.
Area of Science:
- Toxicology
- Reproductive Biology
- Epigenetics
Background:
- Neonicotinoids are widely used insecticides linked to bee population decline.
- Concerns exist regarding potential human and animal exposure to neonicotinoids.
- Thiacloprid (thia) is a neonicotinoid insecticide with potential reproductive effects.
Purpose of the Study:
- To investigate the effects of thiacloprid (thia) on the male reproductive system in mice.
- To analyze morphological, cytological, and molecular changes in testes following gestational exposure.
Main Methods:
- Pregnant mice were exposed to varying doses of thiacloprid (thia) during critical embryonic development periods.
- Adult male offspring testes were examined using histological staining (H&E).
- Immunofluorescence, Western blotting, RT-qPCR, and RNA-seq were employed to assess molecular impacts.
Main Results:
- Thiacloprid (thia) exposure decreased sperm count and induced telomere defects at tested doses.
- Increased meiotic pachytene cells and reduced lumen size were observed at higher doses.
- RNA-seq revealed deregulation of genes involved in translation, ATP production, and chromatin modification, alongside decreased H3K9me3 levels and increased retroelement activity.
Conclusions:
- Gestational exposure to thiacloprid (thia) impacts epigenetic mechanisms governing meiosis.
- These disruptions can lead to adverse effects on male spermatogenesis.
- Thiacloprid (thia) poses a risk to male reproductive health through epigenetic alterations.
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