Aryl hydrocarbon receptor-mediated apoptosis of neuronal cells: a possible interaction with estrogen receptor signaling
Abstract
Activation of aryl hydrocarbon receptors (AhRs) induces neuronal damage, but the mechanism by which this occurs is largely unknown. This study evaluated the effects of an AhR agonist, beta-naphthoflavone, on apoptotic pathways in mouse primary neuronal cell cultures. beta-Naphthoflavone (0.1-100 micronhanced caspase-3 activity and lactate dehydrogenase (LDH) release in neocortical and hippocampal cells. These data were supported at the cellular level with Hoechst 33342 and calcein AM staining. alpha-Naphthoflavone inhibited the action of beta-naphthoflavone, thus confirming specific activation of AhRs. A high-affinity estrogen receptor (ER) antagonist, ICI 182,780, and a selective estrogen receptor modulator (SERM), tamoxifen, enhanced beta-naphthoflavone-mediated apoptosis. Another SERM, raloxifene, and an ERalpha antagonist, methyl-piperidino-pyrazole, did not affect beta-naphthoflavone-induced caspase-3 activity. However, they inhibited beta-naphthoflavone-induced LDH release at a late hour of treatment, thus suggesting delayed control of AhR-mediated neuronal cell death. The apoptotic effects of beta-naphthoflavone were accompanied by increased levels of AhRs, and these receptors colocalized with ERbeta as demonstrated by confocal microscopy. These data strongly support apoptotic effects of AhR activation in neocortical and hippocampal tissues. Moreover, this study provides evidence for direct interaction of the AhR-mediated apoptotic pathway with estrogen receptor signal…
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DBP and related compounds are antiandrogenic but also interact with PPARγ and AhR, thereby affecting transcriptional regulation, apoptosis, and neurodevelopmental programming.
“DBP and related compounds are best known for their antiandrogenic activity, but they also interact with peroxisome proliferator-activated receptors, particularly peroxisome proliferator-activated receptor gamma (PPARγ), and with the aryl hydrocarbon receptor (AhR), thereby affecting transcriptional regulation, apoptosis, and neurodevelopmental programming (Kajta et al., 2009; Wójtowicz et al., 201”
From Environmental endocrine disruptors at the synapse: mechanisms linking chemical exposure to cognitive and behavioral dysfunction (2026) · cites this paper as Kajta et al., 2009
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References 47 · Cited by 70
- Authors
- Kajta, M., Wójtowicz, A. K., Maćkowiak, M., & Lasoń, W.
- Affiliations
- Maj Institute of Pharmacology (PL)
- Jagiellonian University (PL)
- Corresponding author
- Kajta, M.
- Venue
- Neuroscience
- Publisher
- Elsevier BV
- Published
- 2009-01
- Volume
- 158
- Issue
- 2
- Pages
- 811-822
- ISSN
- 0306-4522 (ISSN-L)
- OpenAlex
- W1979379615
- Cited by
- 70
- References
- 47
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 3 · 2023: 3 · 2022: 2 · 2021: 6 · 2020: 2 · 2019: 2 · 2018: 7 · 2017: 2 · 2016: 4 · 2015: 6 · 2014: 8 · 2013: 9
- FWCI
- 2.30
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Instytut Farmakologii im. Jerzego Maja Polskiej Akademii Nauk
- Ministerstwo Edukacji i Nauki (2P05A 123 30)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- aryl hydrocarbon receptor, beta-naphthoflavone, neuronal apoptosis, estrogen receptor signaling, caspase-3, lactate dehydrogenase release, selective estrogen receptor modulators, tamoxifen, fulvestrant, raloxifene, estrogen receptor beta, neurotoxicity, hippocampal neurons, neocortical neurons, receptor colocalization
- MeSH terms
- Animals, Cells, Cultured, Dose-Response Relationship, Drug, Embryo, Mammalian, Enzyme Inhibitors, Estrogen Antagonists, Fluoresceins, Hippocampus, L-Lactate Dehydrogenase, Neurons, Receptors, Estrogen, Tamoxifen, Time Factors, Signal Transduction, Apoptosis, Receptors, Aryl Hydrocarbon, beta-Naphthoflavone, Neocortex, Selective Estrogen Receptor Modulators, Mice, Caspase 3
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