PUBLICATION
Early-life exposure to tris (1,3-dichloro-2-propyl) phosphate caused multigenerational neurodevelopmental toxicity in zebrafish via altering maternal thyroid hormones transfer and epigenetic modifications
- Authors
- Li, R., Yang, L., Han, J., Zou, Y., Wang, Y., Feng, C., Zhou, B.
- ID
- ZDB-PUB-210604-6
- Date
- 2021
- Source
- Environmental pollution (Barking, Essex : 1987) 285: 117471 (Journal)
- Registered Authors
- Yang, LiHua, Zhou, BingSheng
- Keywords
- DNA methylation, Maternal THs transfer, Neurodevelopmental toxicity, TDCIPP, Zebrafish
- MeSH Terms
-
- Animals
- Epigenesis, Genetic
- Female
- Flame Retardants*/toxicity
- Humans
- Larva/metabolism
- Male
- Monocarboxylic Acid Transporters
- Organophosphorus Compounds
- Phosphates/metabolism
- Symporters*
- Thyroid Hormones
- Water Pollutants, Chemical*/toxicity
- Zebrafish/metabolism
- PubMed
- 34082372 Full text @ Environ. Pollut.
Citation
Li, R., Yang, L., Han, J., Zou, Y., Wang, Y., Feng, C., Zhou, B. (2021) Early-life exposure to tris (1,3-dichloro-2-propyl) phosphate caused multigenerational neurodevelopmental toxicity in zebrafish via altering maternal thyroid hormones transfer and epigenetic modifications. Environmental pollution (Barking, Essex : 1987). 285:117471.
Abstract
Tris (1,3-dichloro-2-propyl) phosphate (TDCIPP), an alternative to brominated flame retardants, might pose an exposure risk to humans and wild animals during fetal development. Our recent study suggested that short-term TDCIPP exposure during early development caused sex-dependent behavioral alteration in adults. In the present study, multigenerational neurodevelopmental toxicity upon early-life exposure of parental zebrafish was evaluated, and the possible underlying mechanisms were further explored. Specifically, after embryonic exposure (0-10 days post-fertilization, dpf) to TDCIPP (0, 0.01, 0.10, and 1.00 μM), zebrafish larvae were cultured in clean water until the sexually matured to produce progeny (F1). The results confirmed neurodevelopmental toxicity in F1 larvae characterized by changes of developmental endpoints, reduced thigmotaxis, as well as altered transcription of genes including myelin basic protein a (mbpa), growth associated protein (gap43) and synapsin IIa (syn2a). Sex-specific changes in thyroid hormones (THs) indicated the relationship of abnormal THs levels with previously reported neurotoxicity in adult females after early-life exposure to TDCIPP. Similar changing profiles of TH levels (increased T3 and decreased T4) in adult females and F1 eggs, but not in F1 larvae, suggested that the TH disruptions were primarily inherited from the maternal fish. Further results demonstrated hypermethylation of global DNA and key genes related to TH transport including transthyretin (ttr) and solute carrier family 16 member 2 (slc16a2), which might affect the transport of THs to target tissues, thus at least partially contributing to the neurodevelopmental toxicity in F1 larvae. Overall, our results confirmed that early-life TDCIPP exposure of parental fish could affect the early neurodevelopment of F1 offspring. The underlying mechanism could involve altered TH levels inherited from maternal zebrafish and epigenetic modifications in F1 larvae.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping