ArticleToxicology reports2024
The epoxiconazole and tebuconazole fungicides impair granulosa cells functions partly through the aryl hydrocarbon receptor (AHR) signalling with contrasted effects in obese, normo-weight and polycystic ovarian syndrome (PCOS) patients.
Article in Toxicology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- The role of the aryl hydrocarbon receptor in ovarian development, function, xenobiotic metabolism, and disease†.Biology of reproduction · 2026Review
- A review on herbal interventions and nanotechnological advancements for managing polycystic ovarian syndrome.JBRA assisted reproduction · 2025Review
- A Systematic Review on the Toxicology of European Union-Approved Triazole Fungicides in Cell Lines and Mammalian Models.Journal of xenobiotics · 2025Review
- Adverse Effects of Pesticides on the Ovary: Evidence from Epidemiological and Toxicological Studies.Environment & health (Washington, D.C.) · 2025Review
- Understanding the impact of triazoles on female fertility and embryo development: Mechanisms and implications.Toxicology reports · 2025Review
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Authors and funding
13 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polycystic ovarian syndrome (PCOS), frequently associated to obesity, is the main reproductive disorder in women in age to procreate. Some evidence suggests that pesticides can result in alterations of the female reproductive system, including polycystic ovary syndrome (PCOS). Here, we detected two fungicides, Tebuconazole (Tb) and Epoxiconazole (Epox) in the soils and waters of French area. Our hypothesis is that these two triazoles could be associated to the etiology of PCOS. We used the human KGN cell line and primary human granulosa cells (hGCs) from different group of patients: normal weight non PCOS (NW), normal weight PCOS (PCOS NW), obese (obese) and obese PCOS (PCOS obese). We exposed in vitro these cells to Tb and Epox from 0 up to 10 mM for 24 and 48 h and analysed cell viability and steroidogenesis. In hGCs NW, cell viability was reduced from 12.5 µM for Tb and 75 µM for Epox. In hGCs NW, Epox decreased progesterone (Pg) and estradiol (E2) secretions and inhibited
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