High dose bisphenol A impairs hippocampal neurogenesis in female mice across generations
Open accessAbstract
Bisphenol A (BPA) is used as a monomer during the manufacture of polycarbonate plastics and epoxy resins. However, BPA adversely affects reproductive organ growth and development, and it has been proposed that the detrimental effects of BPA could extend to future generations. The present study was conducted to evaluate the transgenerational effects of BPA on hippocampal neurogenesis and neurocognitive function. Pregnant female C57BL/6 mice (F0) were exposed to BPA (0.1-10 mg/kg) from gestation day 6 to 17, and female offspring (F2) from F1 generation mice were prepared. It was found that exposure of F0 mice to BPA at 10 mg/kg decreased the number of newly generated cells in the hippocampi of F2 female mice. Passive avoidance testing revealed that high-doses BPA (1 mg/kg and 10 mg/kg) decreased cross-over latency time in F2 mice, suggesting a BPA-mediated neurocognitive deficit in terms of memory retention. Furthermore, it was found that levels of phospho-ERK, brain-derived neurotrophic factor (BDNF), and phospho-CREB in hippocampi were significantly lower in F2 mice. Interestingly, the effects of BPA on hippocampal neurogenesis were found to be correlated with altered DNA methylation. In particular, high-dose BPA exposure increased DNA methylation of the CREB regulated transcription coactivator 1 (Crtc1) generated in F2 mice. These findings suggest that BPA exposure of pregnant mothers could adversely affect hippocampal neurogenesis and cognitive function in future generations by modulating the ERK and BDNF-CREB signaling cascades.
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BPA declined neurogenesis in DG.
“Another reason for BPA induced spatial memory deficits may be that BPA declined neurogenesis in DG2734.”
High-dose BPA exposure to pregnant mice affects hippocampal neurogenesis and memory retention in the second generation.
“It has been reported that high-dose BPA exposure to pregnant mice affects hippocampal neurogenesis and memory retention in the second generation, which have no experience of BPA exposure27.”
BPA exposure during early development has a long-lasting impact.
“the result suggested that BPA exposure during early development have a long-lasting impact.”
Female F2 descendents of mice exposed to BPA (1, 10 mg/kg) on GD6-17 displayed a decreased number of newly generated hippocampal cells compared with vehicle lines.
“Female F2 descendents of mice exposed to BPA (1, 10 mg/kg) on GD6-17 displayed a decreased number of newly generated hippocampal cells compared with vehicle lines [ 149 ].”
From DNA methylation: a mechanism linking environmental chemical exposures to risk of autism spectrum disorders? (2016) · cites this paper as [149]
These mice also displayed deficits in brain-derived neurotrophic factor (BDNF), phosphorylated cAMP response element binding protein (p-CREB) and phosphorylated extracellular signal-regulated kinase, which were accompanied by changes in DNA methylation of the CREB regulated transcription factor coactivator 1 gene.
“These mice also displayed deficits in brain-derived neurotrophic factor (BDNF), phosphorylated cAMP response element binding protein (p-CREB) and phosphorylated extracellular signal-regulated kinase, which were accompanied by changes in DNA methylation of the CREB regulated transcription factor coactivator 1 gene [ 149 ].”
From DNA methylation: a mechanism linking environmental chemical exposures to risk of autism spectrum disorders? (2016) · cites this paper as [149]
This change was associated with deficits in learning and memory.
“This change was associated with deficits in learning and memory.”
From DNA methylation: a mechanism linking environmental chemical exposures to risk of autism spectrum disorders? (2016) · cites this paper as [149]
Although Morris water maze testing did not reveal significant differences between treatment groups, F2 mice of the BPA lineage did exhibit reduced cross over latency in passive avoidance testing, suggesting impaired ability to remember past foot shock.
“Although Morris water maze testing did not reveal significant differences between treatment groups, F2 mice of the BPA lineage did exhibit reduced cross over latency in passive avoidance testing, suggesting impaired ability to remember past foot shock [ 149 ].”
From DNA methylation: a mechanism linking environmental chemical exposures to risk of autism spectrum disorders? (2016) · cites this paper as [149]
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References 42 · Cited by 82
- Authors
- Jang, Y. J., Park, H. R., Kim, T. H., Yang, W.-J., Lee, J.-J., Choi, S. Y., Oh, S. B., Lee, E., Park, J.-H., Kim, H.-P., Kim, H. S., & Lee, J.
- Affiliations
- Pusan National University (KR)
- Yonsei University (KR)
- Corresponding author
- Lee, Jaewon
- ORCID
- Venue
- Toxicology
- Publisher
- Elsevier BV
- Published
- 2012-06
- Volume
- 296
- Issue
- 1-3
- Pages
- 73-82
- ISSN
- 0300-483X (ISSN-L)
- OpenAlex
- W2024345203
- Cited by
- 82
- References
- 42
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 3 · 2023: 4 · 2022: 5 · 2021: 3 · 2020: 6 · 2019: 8 · 2018: 10 · 2017: 7 · 2016: 6 · 2015: 5 · 2014: 12 · 2013: 5 · 2012: 2
- FWCI
- 5.31
- Type
- journal article
- Language
- en
- Open access
- Licence
- Locations
- Toxicology (publishedVersion)
- PubMed (publishedVersion)
- YUHSpace (Yonsei University Medical Library) (submittedVersion, cc-by-nc-nd)
- Funders
- National Institute of Food and Drug Safety Evaluation, Korea FDA (101622 EDS 651)
- MEST (20090083538)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Keywords
- bisphenol A, hippocampal neurogenesis, transgenerational effects, maternal exposure, neurocognitive impairment, memory retention, DNA methylation, CRTC1, ERK signaling, endocrine disruptors, female offspring
- MeSH terms
- Bisphenol A Compounds, Animals, Benzhydryl Compounds, Cognition, Estrogens, Non-Steroidal, Female, Hippocampus, Learning, Maternal-Fetal Exchange, Mice, Inbred C57BL, Phenols, Pregnancy, Cyclic AMP Response Element-Binding Protein, Brain-Derived Neurotrophic Factor, Mice, Endocrine Disruptors, Neurogenesis
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