ArticleProceedings of the National Academy of Sciences of the United States of America2015
Low-dose exposure to bisphenol A and replacement bisphenol S induces precocious hypothalamic neurogenesis in embryonic zebrafish.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers, 1 of them a synthesis that pooled it.
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Who cites it
136 citing papers in PubMed, 1 synthesis or guideline pooled it, 465 citations in OpenAlex.
- Bisphenol A exposure and children's behavior: A systematic review.Journal of exposure science & environmental epidemiology · 2017Pooled it
- Beyond medication adherence: bisphenol exposure and its relationship with good glycemic control in type 2 diabetes.Acta diabetologica · 2026Article
- Article
- Embryonic exposure to environmental levels of roundup affects neurodevelopment in zebrafish.Journal of the Endocrine Society · 2026Article
- An Integrated Approach Combining Regulatory Tests inEnvironmental science & technology · 2026Article
- Bisphenol S and Neurological Health: An Integrated Overview of Neurotoxicity and Underlying Mechanisms.Molecular neurobiology · 2026Review
- Dietary Glyphosate Exposure Disrupts Hepatic and Reproductive Function in Female Zebrafish at Regulatory Safe Levels.Toxics · 2026Article
- Intrauterine Exposure to Endocrine-disrupting Chemicals and Risk of Hypospadias: A Pilot Study.Journal of the Endocrine Society · 2026Article
- Replacing BPA: Structural Substitutes BPAF Binding to the Progesterone Receptor Elevates Breast Cancer Risk.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Environmental endocrine disruptors at the synapse: mechanisms linking chemical exposure to cognitive and behavioral dysfunction.Frontiers in behavioral neuroscience · 2026Review
- Disruption of estrogen signaling by developmental exposure to BPA and TBT causes long term functional deficits in zebrafish retina.Frontiers in pharmacology · 2026Review
- Article
- Bisphenol A and Its Analogue Bisphenol S Inhibit Cholinergic Neurotransmission at the Tripartite Colonic Myenteric Synapse of CD1 Mice by Targeting Interstitial Cells of Cajal.International journal of molecular sciences · 2025Article
- Reproductive Risk Assessment of Bisphenol A and Its Substitutes on Estrogen Receptors (ERs) in Bivalves.International journal of molecular sciences · 2025Article
- Mutation of Brain Aromatase Impairs Behavior and Neuroplasticity in Adult Zebrafish.Journal of neurochemistry · 2025Article
- Loss of adult visual responses by developmental BPA exposure is correlated with altered estrogenic signaling.Communications biology · 2025Article
- Developmental neurotoxicity of bisphenol F and bisphenol S in animal model systems: A literature review.Neurotoxicology · 2025Review
- Article
- Genetic and Environmental Factors Co-Contributing to Behavioral Abnormalities inInternational journal of molecular sciences · 2024Article
- Gestational bisphenol A exposure alters energy homeostasis and adult hypothalamic neurogenesis in female mice.Scientific reports · 2024Article
76 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bisphenol A (BPA), a ubiquitous endocrine disruptor that is present in many household products, has been linked to obesity, cancer, and, most relevant here, childhood neurological disorders such as anxiety and hyperactivity. However, how BPA exposure translates into these neurodevelopmental disorders remains poorly understood. Here, we used zebrafish to link BPA mechanistically to disease etiology. Strikingly, treatment of embryonic zebrafish with very low-dose BPA (0.0068 μM, 1,000-fold lower than the accepted human daily exposure) and bisphenol S (BPS), a common analog used in BPA-free products, resulted in 180% and 240% increases, respectively, in neuronal birth (neurogenesis) within the hypothalamus, a highly conserved brain region involved in hyperactivity. Furthermore, restricted BPA/BPS exposure specifically during the neurogenic window caused later hyperactive behaviors in zebrafish larvae. Unexpectedly, we show that BPA-mediated precocious neurogenesis and the concomitant behavioral phenotype were not dependent on predicted estrogen receptors but relied on androgen receptor-mediated up-regulation of aromatase. Although human epidemiological results are still emerging, an association between high maternal urinary BPA during gestation and hyperactivity and other behavioral disturbances in the child has been suggested. Our studies here provide mechanistic support that the neurogenic period indeed may be a window of vulnerability and uncovers previously unexplored avenues of research into how endocrine disruptors might perturb early brain development. Furthermore, our results show that BPA-free products are not necessarily safer and support the removal of all bisphenols from consumer merchandise.
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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.