PUBLICATION

Transgenerational endocrine disruption and neurotoxicity in zebrafish larvae after parental exposure to binary mixtures of decabromodiphenyl ether (BDE-209) and lead

Authors
Chen, L., Wang, X., Zhang, X., Lam, P.K.S., Guo, Y., Lam, J.C.W., Zhou, B.
ID
ZDB-PUB-170627-7
Date
2017
Source
Environmental pollution (Barking, Essex : 1987)   230: 96-106 (Journal)
Registered Authors
Guo, YongYong, Zhou, BingSheng
Keywords
BDE-209, Chronic coexposure, Pb, Transgenerational effects, Zebrafish
MeSH Terms
  • Animals
  • Endocrine Disruptors/toxicity*
  • Halogenated Diphenyl Ethers/metabolism
  • Halogenated Diphenyl Ethers/toxicity*
  • Larva/drug effects
  • Lead/metabolism
  • Lead/toxicity*
  • Nervous System/drug effects*
  • Thyroid Gland/metabolism
  • Toxicity Tests
  • Water Pollutants, Chemical/toxicity*
  • Zebrafish/metabolism
  • Zebrafish/physiology*
PubMed
28649046 Full text @ Environ. Pollut.
Abstract
Polybrominated diphenyl ethers (PBDEs) and heavy metals are two key groups of electric and electronic equipment contaminants. Despite their co-occurrence in aquatic environments, their combined effects remain largely unknown, particularly under a chronic exposure regime. In the present study, adult zebrafish (Danio rerio) were exposed to environmentally relevant concentrations of BDE-209 and lead (Pb), or their binary mixtures, for 3 months. After chronic parental exposure, increased transfer of BDE-209 and Pb to the offspring eggs was activated in the coexposure groups, with BDE-197 being the predominant PBDE congener, indicating the dynamic metabolism of BDE-209 in parental zebrafish. In the presence of Pb, culturing the eggs in clean water until 5 days post-fertilization (dpf) further accelerated the debromination of BDE-209 towards BDE-197 in the offspring, caused by the preferential removal of bromine atoms at meta positions. BDE-209 and Pb combinations induced reproductive and thyroid endocrine disruption in adults, which resulted in an imbalanced deposition of hormones in the eggs. However, compared with single chemical exposure, the larval offspring at 5 dpf from the coexposure groups had reversed the adverse influences from maternal origin. In addition, the interaction between BDE-209 and Pb led to transgenerational developmental neurotoxicity in the larval offspring, where inhibited neuronal growth and neurotransmitter signaling, disorganized muscular assembly, and impaired visual function contributed to the observed neurobehavioral deficits. Overall, depending on specific biological events, the complex interaction between BDE-209 and Pb under chronic exposure resulted in significant alterations in their environmental fate and toxicological actions, thus complicating the accurate evaluation of ecological risks and constituting an unquantified threat to environmental safety.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping