ArticleChemical research in toxicology2015
Disruption of type 2 iodothyronine deiodinase activity in cultured human glial cells by polybrominated diphenyl ethers.
Article in Chemical research in toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 48 citations in OpenAlex.
- Update of the risk assessment of polybrominated diphenyl ethers (PBDEs) in food.EFSA journal. European Food Safety Authority · 2024Article
- Toxic Effects and Mechanisms of Polybrominated Diphenyl Ethers.International journal of molecular sciences · 2023Review
- Endocrine disrupting and carcinogenic effects of decabromodiphenyl ether.Frontiers in endocrinology · 2023Review
- Mechanisms of Male Reproductive Toxicity of Polybrominated Diphenyl Ethers.International journal of molecular sciences · 2022Review
- Plasticizers: negative impacts on the thyroid hormone system.Environmental science and pollution research international · 2022Review
- A Halogen Bonding Perspective on Iodothyronine Deiodinase Activity.Molecules (Basel, Switzerland) · 2020Review
- Inhibition of Human Liver Carboxylesterase (hCE1) by Organophosphate Ester Flame Retardants and Plasticizers: Implications for Pharmacotherapy.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Screening the ToxCast Phase 1, Phase 2, and e1k Chemical Libraries for Inhibitors of Iodothyronine Deiodinases.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Polybrominated diphenyl ether (PBDE) exposures and thyroid hormones in children at age 3 years.Environment international · 2018Article
- Halogen Bonding from the Bonding Perspective with Considerations for Mechanisms of Thyroid Hormone Activation and Inhibition.New journal of chemistry = Nouveau journal de chimie · 2018Article
- Thyroid-disrupting chemicals and brain development: an update.Endocrine connections · 2018Review
- Associations between serum polybrominated diphenyl ethers and thyroid hormones in a cross sectional study of a remote Alaska Native population.Scientific reports · 2018Article
- Organ-on-a-chip for assessing environmental toxicants.Current opinion in biotechnology · 2017Review
- Brominated flame retardants in placental tissues: associations with infant sex and thyroid hormone endpoints.Environmental health : a global access science source · 2016Article
- Serum polybrominated diphenyl ether concentrations and thyroid function in young children.Environmental research · 2016Article
- Toxic chemicals and thyroid function: hard facts and lateral thinking.Reviews in endocrine & metabolic disorders · 2015Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Polybrominated diphenyl ether (PBDE) flame retardants are endocrine disruptors and suspected neurodevelopmental toxicants. While the direct mechanisms of neurodevelopmental toxicity have not been fully elucidated, it is conceivable that alterations in thyroid hormone levels in the developing brain may contribute to these effects. Cells within the brain locally convert thyroxine (T4) to the biologically active triiodothyronine (T3) through the action of the selenodeiodinase type 2 iodothyronine deiodinase (DIO2). Previous studies have demonstrated that PBDEs can alter hepatic deiodinase activity both in vitro and in vivo; however, the effects of PBDEs on the deiodinase isoforms expressed in the brain are not well understood. Here, we studied the effects of several individual PBDEs and hydroxylated metabolites (OH-BDEs) on DIO2 activity in astrocytes, a specialized glial cell responsible for production of more than 50% of the T3 required by the brain. Primary human astrocytes and H4 glioma cells were exposed to individual PBDEs or OH-BDEs at concentrations up to 5 μM. BDE-99 decreased DIO2 activity by 50% in primary astrocyte cells and by up to 80% in the H4 cells at doses of ≥500 nM. 3-OH-BDE-47, 6-OH-BDE-47, and 5'-OH-BDE-99 also decreased DIO2 activity in cultured H4 glioma cells by 45-80% at doses of approximately 1-5 μM. Multiple mechanisms appear to contribute to the decreased DIO2 activity, including weakened expression of DIO2 mRNA, competitive inhibition of DIO2, and enhanced post-translational degradation of DIO2. We conclude that decreases in DIO2 activity caused by exposure to PBDEs may play a role in the neurodevelopmental deficits caused by these toxicants.
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