ArticleBiology of reproduction2012
Bisphenol A inhibits follicle growth and induces atresia in cultured mouse antral follicles independently of the genomic estrogenic pathway.
Article in Biology of reproduction, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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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
38 citing papers in PubMed, 105 citations in OpenAlex.
- Bisphenol-A and human oocyte maturation in vitro.Human reproduction (Oxford, England) · 2013Trial
- Review
- Reproductive Effects of Endocrine Disruptors in Domestic Ruminants: Integrating In Vitro and In Vivo Evidence.Animals : an open access journal from MDPI · 2025Review
- Developmental programming: mechanisms of early exposure to real-life chemicals in biosolids on offspring ovarian dynamics†.Biology of reproduction · 2025Article
- Protective effects of apricot kernel oil and metformin against BPA-induced ovarian toxicity in rat models of polycystic ovary syndrome: insights into PI3K/AKT and mitochondrial apoptosis pathways.Toxicology research · 2025Article
- The deleterious effect of bisphenol S on early embryo development of mice.Hormones (Athens, Greece) · 2025Article
- Rapid identification of reproductive toxicants among environmental chemicals using an in vivo evaluation of gametogenesis in budding yeast Saccharomyces cerevisiae.Reproductive toxicology (Elmsford, N.Y.) · 2024Article
- Toxicological Impact of Bisphenol A on Females' Reproductive System: Review Based on Experimental and Epidemiological Studies.Reproductive sciences (Thousand Oaks, Calif.) · 2024Review
- Genetic and Epigenetic Profiles of Polycystic Ovarian Syndrome and In Vitro Bisphenol Exposure in a Human Granulosa Cell Model.Biomedicines · 2024Article
- Interference Mechanisms of Endocrine System and Other Systems of Endocrine-Disrupting Chemicals in Cosmetics-In Vitro Studies.International journal of endocrinology · 2024Review
- Bisphenols A and F, but not S, induce apoptosis in bovine granulosa cellsFrontiers in endocrinology · 2022Article
- BPA and BPS affect the expression of anti-Mullerian hormone (AMH) and its receptor during bovine oocyte maturation and early embryo development.Reproductive biology and endocrinology : RB&E · 2021Article
- Environmentally relevant mixtures of phthalates and phthalate metabolites differentially alter the cell cycle and apoptosis in mouse neonatal ovaries†.Biology of reproduction · 2021Article
- Article
- Epigenetic effects of Bisphenol A on granulosa cells of mouse follicles during in vitro culture: An experimental study.International journal of reproductive biomedicine · 2021Article
- Data integration, analysis, and interpretation of eight academic CLARITY-BPA studies.Reproductive toxicology (Elmsford, N.Y.) · 2020Article
- Environmental toxicant exposure and menstrual cycle length.Current opinion in endocrinology, diabetes, and obesity · 2020Review
- Bisphenol A: an emerging threat to female fertility.Reproductive biology and endocrinology : RB&E · 2020Review
- The effects of in utero bisphenol A exposure on ovarian follicle numbers and steroidogenesis in the F1 and F2 generations of mice.Reproductive toxicology (Elmsford, N.Y.) · 2017Article
- Bisphenol A Exposure, Ovarian Follicle Numbers, and Female Sex Steroid Hormone Levels: Results From a CLARITY-BPA Study.Endocrinology · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Bisphenol A (BPA) is an estrogenic chemical used to manufacture many commonly used plastic and epoxy resin-based products. BPA ubiquitously binds to estrogen receptors throughout the body, including estrogen receptor alpha (ESR1) in the ovary. Few studies have investigated the effects of BPA on ovarian antral follicles. Thus, we tested the hypothesis that BPA alters cell cycle regulators and induces atresia in antral follicles via the genomic estrogenic pathway, inhibiting follicle growth. To test this hypothesis, we isolated antral follicles from 32- to 35-day-old control and Esr1-overexpressing mice and cultured them with vehicle control (dimethylsulfoxide [DMSO]) or BPA (1-100 μg/ml). Additionally, antral follicles were isolated from 32- to 35-day-old FVB mice and cultured with DMSO, BPA (1-100 μg/ml), estradiol (10 nM), ICI 182,780 (ICI; 1 μM), BPA plus ICI, or BPA plus estradiol. Follicles were measured for growth every 24 h for 96-120 h and processed either for analysis of estrogen receptor, cell cycle, and/or atresia factor mRNA expression, or for histological evaluation of atresia. Results indicate that estradiol and ICI do not protect follicles from BPA-induced growth inhibition and that estradiol does not protect follicles from BPA-induced atresia. Furthermore, overexpressing Esr1 does not increase susceptibility of follicles to BPA-induced growth inhibition. Additionally, BPA up-regulates Cdk4, Ccne1, and Trp53 expression, whereas it down-regulates Ccnd2 expression. BPA also up-regulates Bax and Bcl2 expression while inducing atresia in antral follicles. These data indicate that BPA abnormally regulates cell cycle and atresia factors, and this may lead to atresia and inhibited follicle growth independently of the genomic estrogenic pathway.
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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.