ArticleEnvironmental health perspectives2019
Environmentally Relevant Perinatal Exposures to Bisphenol A Disrupt Postnatal Kiss1/NKB Neuronal Maturation and Puberty Onset in Female Mice.
Article in Environmental health perspectives, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 53 citations in OpenAlex.
- Hypothalamic control of puberty: from neuronal circuits to mechanisms for its metabolic regulation.Reviews in endocrine & metabolic disorders · 2026Review
- A computational analysis of multi-target mechanisms linking bisphenol A to precocious puberty.PeerJ · 2026Article
- Endocrine-disrupting chemicals and female reproductive health: a growing concern.Nature reviews. Endocrinology · 2025Review
- EndoCompass Project: Environmental Endocrinology.Hormone research in paediatrics · 2025Review
- Maternal Bisphenol B Exposure and Mammary Gland Development of Offspring: A Time-Series Analysis.Environment & health (Washington, D.C.) · 2023Article
- Cocktails of NSAIDs and 17α Ethinylestradiol at Environmentally Relevant Doses in Drinking Water Alter Puberty Onset in Mice Intergenerationally.International journal of molecular sciences · 2023Article
- Review
- Dicer ablation in Kiss1 neurons impairs puberty and fertility preferentially in female mice.Nature communications · 2022Article
- Early programming of reproductive health and fertility: novel neuroendocrine mechanisms and implications in reproductive medicine.Human reproduction update · 2022Review
- Epigenetic regulation of 5α reductase-1 underlies adaptive plasticity of reproductive function and pubertal timing.BMC biology · 2022Article
- Emerging Roles of Epigenetics in the Control of Reproductive Function: Focus on Central Neuroendocrine Mechanisms.Journal of the Endocrine Society · 2021Review
- REPRODUCTIVE TOXICOLOGY: Endocrine disruption and reproductive disorders: impacts on sexually dimorphic neuroendocrine pathways.Reproduction (Cambridge, England) · 2021Review
- Transgenerational effects of polychlorinated biphenyls: 2. Hypothalamic gene expression in rats†.Biology of reproduction · 2021Article
- Multi- and Transgenerational Outcomes of an Exposure to a Mixture of Endocrine-Disrupting Chemicals (EDCs) on Puberty and Maternal Behavior in the Female Rat.Environmental health perspectives · 2021Article
- Early Postnatal Genistein Administration Affects Mice Metabolism and Reproduction in a Sexually Dimorphic Way.Metabolites · 2021Article
- EDCs Reorganize Brain-Behavior Phenotypic Relationships in Rats.Journal of the Endocrine Society · 2021Article
- Cellular and molecular features of EDC exposure: consequences for the GnRH network.Nature reviews. Endocrinology · 2021Review
- Bisphenol A and Puberty Onset in Female Mice: Developmental Effects of Low-Dose Exposure.Environmental health perspectives · 2020Article
- Endocrine disruption of gene expression and microRNA profiles in hippocampus and hypothalamus of California mice: Association of gene expression changes with behavioural outcomes.Journal of neuroendocrinology · 2020Article
- THE EFFECTS OF ENDOCRINE DISRUPTORS ON FEMALE GONADAL AXIS: AN UPDATE.Acta endocrinologica (Bucharest, Romania : 2005)Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe timing of puberty is highly sensitive to environmental factors, including endocrine disruptors. Among them, bisphenol A (BPA) has been previously analyzed as potential modifier of puberty. Yet, disparate results have been reported, with BPA advancing, delaying, or being neutral in its effects on puberty onset. Likewise, mechanistic analyses addressing the central and peripheral actions/targets of BPA at puberty remain incomplete and conflictive.
objectiveWe aimed to provide a comprehensive characterization of the impact of early BPA exposures, especially at low, real-life doses, on the postnatal development of hypothalamic Kiss1/NKB neurons, and its functional consequences on female pubertal maturation.
methodsPregnant CD1 female mice were orally administered BPA at 5, 10, or
resultsPerinatal exposure to BPA, in a range of doses largely below the no observed adverse effect level (NOAEL;
conclusionsOur data attest to the consistent, but divergent, effects of gestational exposures to low concentrations of BPA, via the oral route, on phenotypic and neuroendocrine markers of puberty in female mice, with an unambiguous impact on the developmental maturation not only of Kiss1, but also of the NKB system, both essential regulators of puberty onset. https://doi.org/10.1289/EHP5570.
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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 Socratic graph.