PPAR-γ agonist GW1929 but not antagonist GW9662 reduces TBBPA-induced neurotoxicity in primary neocortical cells

Wojtowicz, Anna K.; Szychowski, Konrad A.; Kajta, Małgorzata

doi:10.1007/s12640-013-9434-z

Cited by 62Toxic Organic Pollutants ImpactPeroxisome Proliferator-Activated ReceptorsEffects and risks of endocrine disrupting chemicals

PPAR-γ agonist GW1929 but not antagonist GW9662 reduces TBBPA-induced neurotoxicity in primary neocortical cells

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Wojtowicz, Anna K., Szychowski, Konrad A., Kajta, Małgorzata·2014·Neurotoxicity Research

DOI 10.1007/s12640-013-9434-zPMC PMC3936120

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Abstract

Tetrabromobisphenol A (2,2-bis(4-hydroxy-3,5-dibromophenyl)propane; TBBPA) is a widely used brominated flame retardant. TBBPA induces neuronal damage, but the mechanism by which this occurs is largely unknown. We studied the possible involvement of peroxisome proliferator-activated receptor gamma (PPAR-γ) in TBBPA-induced apoptosis and toxicity in mouse primary neuronal cell cultures. TBBPA enhanced both, caspase-3 activity and lactate dehydrogenase (LDH) release in neocortical cells after 6 and 24 h of exposition. These data were supported at the cellular level with Hoechst 33342 staining. Immunoblot analyses showed that, compared with control cells, 10 μM TBBPA decreased the expression of PPAR-γ protein in neocortical neurons after 1-24 h of exposure. Co-treatment with TBBPA and GW1929 inhibited the TBBPA-induced caspase-3 activity, apoptotic body formation, and LDH release as well as TBBPA-induced decrease in PPAR-γ protein expression. Thus, our data support neuroprotective potential of PPAR-γ agonists. The PPAR-γ antagonist GW9662 prevented the TBBPA-induced decrease in PPAR-γ protein level, but it potentiated TBBPA-induced apoptotic and neurotoxic effects, which suggest that the mechanism of TBBPA action in neuronal cells is not only PPAR-γ-dependent. Therefore, further studies of the mechanism of TBBPA action in the nervous system are needed.

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At the nuclear receptor level, TBBPA suppresses PPARγ expression in cortical neurons, whereas BEHPP acts as an antagonist of RARα, two mechanisms that can profoundly interfere with neuronal differentiation and synaptic organization.
“At the nuclear receptor level, tetrabromobisphenol A (TBBPA) suppresses PPARγ expression in cortical neurons, whereas bis-(2-ethylhexyl)-phenyl phosphate (BEHPP) acts as an antagonist of the retinoic acid receptor RARα, two mechanisms that can profoundly interfere with neuronal differentiation and synaptic organization (Jia et al., 2022; Wojtowicz et al., 2014).”
From Environmental endocrine disruptors at the synapse: mechanisms linking chemical exposure to cognitive and behavioral dysfunction (2026) · cites this paper as Wojtowicz et al., 2014

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Authors: Wojtowicz, A. K., Szychowski, K. A., & Kajta, M.
Affiliations: University of Agriculture in Krakow (PL)
Maj Institute of Pharmacology (PL)
ORCID: Szychowski, Konrad A.
Kajta, Małgorzata
Venue: Neurotoxicity Research
Publisher: Springer Science and Business Media LLC
Published: 2013-10-17
Volume: 25
Issue: 3
Pages: 311-322
ISSN: 1029-8428 (ISSN-L)
1476-3524
DOI: 10.1007/s12640-013-9434-z
PMC: PMC3936120
OpenAlex: W2093382734
Cited by: 62
References: 54
Citations by year: 2026: 2 · 2025: 2 · 2024: 8 · 2023: 6 · 2022: 6 · 2021: 4 · 2020: 5 · 2019: 4 · 2018: 1 · 2017: 8 · 2016: 4 · 2015: 6 · 2014: 4 · 2013: 2
FWCI: 3.92
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by
creativecommons.org/licenses/by/2.0 (unspecified)
Locations: Neurotoxicity Research (publishedVersion, cc-by)
Europe PMC (PubMed Central) (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
Funders: Uniwersytet Rolniczy im. Hugona Kołłątaja w Krakowie
Topics: Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
Keywords: tetrabromobisphenol A, brominated flame retardants, PPARγ, GW1929, GW9662, neurotoxicity, neuronal apoptosis, caspase-3, neuroprotection, neocortical neurons, PPARγ agonists, PPARγ antagonist
MeSH terms: Anilides, Animals, Benzophenones, Cells, Cultured, Central Nervous System Agents, Dose-Response Relationship, Drug, L-Lactate Dehydrogenase, Neurons, Polybrominated Biphenyls, Time Factors, Tyrosine, Apoptosis, Neuroprotective Agents, Neocortex, Neurotoxicity Syndromes, PPAR gamma, Mice, Caspase 3

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PPAR-γ agonist GW1929 but not antagonist GW9662 reduces TBBPA-induced neurotoxicity in primary neocortical cells

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