ArticleBiology of reproduction2024
The role of the aryl hydrocarbon receptor in mediating the effects of mono(2-ethylhexyl) phthalate in mouse ovarian antral follicles†.
Article in Biology of reproduction, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Advances in bovine oocyte in vitro maturation: mechanisms and strategies.Veterinary research communications · 2026Review
- Effects of Phthalate Metabolite Mixture Exposure on Mouse Oocyte Development.bioRxiv : the preprint server for biology · 2026Article
- The role of the aryl hydrocarbon receptor in ovarian development, function, xenobiotic metabolism, and disease†.Biology of reproduction · 2026Review
- The Cellular Effects of Di(2-ethylhexyl) Phthalate in Non-Malignant Colonic Epithelia Involve Oxidative Stress.International journal of molecular sciences · 2025Article
- Infectious Bronchitis Virus Activates the Aryl Hydrocarbon Receptor During In Vitro Infection.Veterinary sciences · 2025Article
- Prenatal exposure to an environmentally relevant phthalate mixture alters oxidative stress, apoptosis, cell cycle regulators, and steroidogenic factors in the ovaries of F1 mice.Reproductive toxicology (Elmsford, N.Y.) · 2025Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Di(2-ethylhexyl) phthalate (DEHP) is a pervasive environmental toxicant used in the manufacturing of numerous consumer products, medical supplies, and building materials. DEHP is metabolized to mono(2-ethylhexyl) phthalate (MEHP). MEHP is an endocrine disruptor that adversely affects folliculogenesis and steroidogenesis in the ovary, but its mechanism of action is not fully understood. Thus, we tested the hypothesis that the aryl hydrocarbon receptor (AHR) plays a functional role in MEHP-mediated disruption of folliculogenesis and steroidogenesis. CD-1 mouse antral follicles were isolated and cultured with MEHP (0-400 μM) in the presence or absence of the AHR antagonist CH223191 (1 μM). MEHP treatment reduced follicle growth over a 96-h period, and this effect was partially rescued by co-culture with CH223191. MEHP exposure alone increased expression of known AHR targets, cytochrome P450 (CYP) enzymes Cyp1a1 and Cyp1b1, and this induction was blocked by CH223191. MEHP reduced media concentrations of estrone and estradiol compared to control. This effect was mitigated by co-culture with CH223191. Moreover, MEHP reduced the expression of the estrogen-sensitive genes progesterone receptor (Pgr) and luteinizing hormone/choriogonadotropin receptor (Lhcgr) and co-treatment with CH223191 blocked this effect. Collectively, these data indicate that MEHP activates the AHR to impair follicle growth and reduce estrogen production and signaling in ovarian antral follicles.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.