ArticleToxicological sciences : an official journal of the Society of Toxicology2013
Toxicity of the flame-retardant BDE-49 on brain mitochondria and neuronal progenitor striatal cells enhanced by a PTEN-deficient background.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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38 citing papers in PubMed, 54 citations in OpenAlex.
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- Prenatal Nutritional Factors and Neurodevelopmental Disorders: A Narrative Review.Life (Basel, Switzerland) · 2024Review
- Update of the risk assessment of polybrominated diphenyl ethers (PBDEs) in food.EFSA journal. European Food Safety Authority · 2024Article
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- Disrupted brain mitochondrial morphology after in vivo hydrogen sulfide exposure.Scientific reports · 2023Article
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- Adrenal Corticosteroid Perturbation by the Endocrine Disruptor BDE-47 in a Human Adrenocortical Cell Line and Male Rats.Endocrinology · 2021Article
- Brain Atrophy and White Matter Damage Linked to Peripheral Bioenergetic Deficits in the Neurodegenerative Disease FXTAS.International journal of molecular sciences · 2021Article
- Role of PTEN-less in cardiac injury, hypertrophy and regeneration.Cell regeneration (London, England) · 2021Review
- An Overview of the Main Genetic, Epigenetic and Environmental Factors Involved in Autism Spectrum Disorder Focusing on Synaptic Activity.International journal of molecular sciences · 2020Review
- Certain ortho-hydroxylated brominated ethers are promiscuous kinase inhibitors that impair neuronal signaling and neurodevelopmental processes.The Journal of biological chemistry · 2020Article
- Promotion of mitochondrial fusion protects against developmental PBDE-47 neurotoxicity by restoring mitochondrial homeostasis and suppressing excessive apoptosis.Theranostics · 2020Article
- Neurotoxicity of polychlorinated biphenyls and related organohalogens.Acta neuropathologica · 2019Review
- Beyond autophagy: a novel role for autism-linked Wdfy3 in brain mitophagy.Scientific reports · 2018Article
- Impact ofFrontiers in genetics · 2018Article
- Environmental risk factors for autism: an evidence-based review of systematic reviews and meta-analyses.Molecular autism · 2017Review
- Human Excretion of Polybrominated Diphenyl Ether Flame Retardants: Blood, Urine, and Sweat Study.BioMed research international · 2017Article
- Biodegradation of 3-methyldiphenylether (MDE) by Hydrogenophaga atypical strain QY7-2 and cloning of the methy-oxidation gene mdeABCD.Scientific reports · 2016Article
- Altered Bioenergetics in Primary Dermal Fibroblasts from Adult Carriers of the FMR1 Premutation Before the Onset of the Neurodegenerative Disease Fragile X-Associated Tremor/Ataxia Syndrome.Cerebellum (London, England) · 2016Article
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4 authors at 1 institution in 1 country.
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Abstract
Polybrominated diphenyl ethers (PBDEs) represent an important group of flame retardants extensively used, tonnage of which in the environment has been steadily increasing over the past 25 years. PBDEs or metabolites can induce neurotoxicity and mitochondrial dysfunction (MD) through a variety of mechanisms. Recently, PBDEs with < 5 Br substitutions (i.e., 2,2',4,4'-tetrabromodiphenyl ether [BDE-47] and 2,2',4,5'-tetrabromodiphenyl ether [BDE-49]) have gained interest because of their high bioaccumulation. In particular, congeners such as BDE-49 arise as one of the most biologically active, with concentrations typically lower than those observed for BDE-47 in biological tissues; however, its potential to cause MD at biologically relevant concentrations is unknown. To this end, the effect of BDE-49 was studied in brain mitochondria and neuronal progenitor striatal cells (NPC). BDE-49 uncoupled mitochondria at concentrations < 0.1 nM, whereas at > 1 nM, it inhibited the electron transport at Complex V (mixed type inhibition; IC(50) = 6 nM) and Complex IV (noncompetitive inhibition; IC(50) = 40 nM). These concentrations are easily achieved in plasma concentrations considering that BDE-49 (this study, 400-fold) and other PBDEs accumulate 1-3 orders of magnitude in the cells, particularly in mitochondria and microsomes. Similar effects were observed in NPC and exacerbated with PTEN (negative modulator of the PI3K/Akt pathway) deficiency, background associated with autism-like behavior, schizophrenia, and epilepsy. PBDE-mediated MD per se or enhanced by a background that confers susceptibility to this exposure may have profound implications in the energy balance of brain.
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