PBDE developmental effects on embryonic zebrafish

Usenko, Crystal Y.; Robinson, Eleanor M.; Usenko, Sascha; Brooks, Bryan W.; Bruce, Erica D.

doi:10.1002/etc.570

Cited by 103 publications

(85 citation statements)

References 37 publications

(30 reference statements)

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“…PBDEs can cause neurobehavioral alterations in rodent models (Eriksson et al, 2002;Kodavanti et al, 2010). Recently, locomotor behavior was used as an approach to study the neurobehavioral effects of PBDEs in zebrafish (Chen et al, 2012b;Chou et al, 2010;He et al, 2011;Usenko et al, 2011). Our study confirmed that BDE-209 in the presence of nano-TiO 2 induced neurotoxicity in zebrafish.…”

Section: Discussionsupporting

confidence: 80%

Bioconcentration and metabolism of BDE-209 in the presence of titanium dioxide nanoparticles and impact on the thyroid endocrine system and neuronal development in zebrafish larvae

et al. 2014

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Interactions between organic toxicants and nanoparticles (NPs) in the aquatic environment may modify toxicant bioavailability and consequently the toxicant's environmental fate and toxicity. Therefore, we investigated the influence of titanium dioxide NPs (nano-TiO 2 ) on deca-BDE (BDE-209; a polybrominated diphenyl ether congener) bioconcentration, metabolism and its effects on the thyroid endocrine system in zebrafish (Danio rerio) larvae. Zebrafish embryos were exposed to various concentrations of BDE-209 alone or in combination with nano-TiO 2 (0.1 mg/L) until 7-day post-fertilization. Nano-TiO 2 can adsorb BDE-209 and nano-TiO 2 is taken up into developing zebrafish larvae. Chemical measurements showed that BDE-209 was bioconcentrated and metabolized in zebrafish larvae, and BDE-209 uptake was enhanced by nano-TiO 2 . Furthermore, increased BDE-209 metabolites were detected in larvae co-exposed with nano-TiO 2 . BDE-209 exposure significantly increased whole-body thyroid hormone contents (T 3 and T 4 ); T 4 content significantly increased in the larvae co-exposed with nanoTiO 2 . Nano-TiO 2 exposure alone did not induce generation of reactive oxygen species, lipid peroxidative oxidation, gene transcription or thyroid hormone levels. Upregulation of several gene transcriptions (tsh, tg, dio2) in the hypothalamic-pituitary-thyroid axis was also observed. Furthermore, co-exposure of nano-TiO 2 and BDE-209 caused a decrease in locomotion activity and downregulation of specific genes and proteins involved in the central nervous system of developing zebrafish larvae (e.g. myelin basic protein and a1-tubulin). These results indicate nano-TiO 2 enhances BDE-209 bioavailability and metabolism, leading to thyroid endocrine disruption and developmental neurotoxicity in zebrafish.

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Section: Discussionsupporting

confidence: 80%

Bioconcentration and metabolism of BDE-209 in the presence of titanium dioxide nanoparticles and impact on the thyroid endocrine system and neuronal development in zebrafish larvae

et al. 2014

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“…Alterations in neurobehavioral performance have also been reported for killifish (Fundulus heteroclitus) embryos exposed to DE-71 [20]. Recently, behavioral studies have been carried out to examine the neurobehavioral effects of PBDEs in zebrafish [21][22][23]. These studies indicated that behavioral measurement is a sensitive indicator of PBDE-induced neurotoxicity.…”

Section: Introductionmentioning

confidence: 89%

Acute exposure to DE‐71: Effects on locomotor behavior and developmental neurotoxicity in zebrafish larvae

Chen

Huang

et al. 2012

Enviro Toxic and Chemistry

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Abstract-The aim of the present study was to investigate the acute developmental neurotoxicity of polybrominated diphenyl ethers (PBDEs) in zebrafish larvae. From 2 to 120 h postfertilization zebrafish embryos were exposed to 31.0, 68.7, and 227.6 mg/L). The authors studied the locomotor behavior of larvae, involvement of the cholinergic system, and selected gene and protein expressions in the central nervous system. The results showed that low DE-71 concentration caused hyperactivity, whereas higher concentrations decreased activity during the dark period. During the light period, larval activity was significantly reduced in a concentration-dependent manner. In the cholinergic system, acetylcholinesterase activity significantly increased (10.7 and 12.4%) in the 68.7 and 227.6 mg/L exposure groups, respectively, and acetylcholine concentration accordingly decreased (60.5%) in the 227.6 mg/L exposure group. The mRNA expressions of genes encoding myelin basic protein, neuron microtubule protein (a1-tubulin), and sonic hedgehog a were significantly downregulated. Western blotting assay demonstrated that the protein concentration of a1-tubulin was also decreased.Overall, the present study demonstrated that acute exposure to PBDEs can disrupt the neurobehavior of zebrafish larvae and affect cholinergic neurotransmission and neuron development. Environ. Toxicol. Chem. 2012;31:233831: -234431: . # 2012

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“…48,49 Recently, locomotor behavior approaches have also been performed to study the neurobehavioral effects of PBDEs in zebrafish. 29,50 Neurobehavior is an integrated response of many physiological and biochemical processes. Thus, alternations of locomotor behavior could be due to downregulation of AChE gene transcription, the inhibition of AChE activity, alterations of the natural function of genes and proteins, or by direct neurotoxic effects on neuronal cells.…”

Section: Environmental Science and Technologymentioning

confidence: 99%

Prenatal Transfer of Polybrominated Diphenyl Ethers (PBDEs) Results in Developmental Neurotoxicity in Zebrafish Larvae

Chen

Huang

et al. 2012

Environ. Sci. Technol.

160

100

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Parental exposure to polybrominated diphenyl ethers (PBDEs) in animals has been found to be transferred to the offspring. The environmental health risk and toxicity to the offspring are still unclear. The objective of the present study was to identify environmentally relevant concentrations of PBDEs for parental exposure that would cause developmental neurotoxicity in the offspring. Adult zebrafish were exposed to environmentally relevant concentrations of 0.8, 4.0 μg/L) via water. The results showed that PBDE exposure did not affect larvae hatching, malformation, or survival. The residue of PBDEs was detected in F1 eggs upon parental exposure. Acetylcholinesterase (AChE) activity was significantly inhibited in F1 larvae. Genes of central nervous system development (e.g., myelin basic protein, synapsin IIa, α1-tubulin) were significantly downregulated in larvae. Protein levels of α1-tubulin and synapsin IIa were also reduced. Decreased locomotion activity was observed in the larvae. This study provides the first evidence that parental exposure to environmentally relevant concentrations of PBDEs could cause adverse effects on neurodevelopment in zebrafish offspring.

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PBDE developmental effects on embryonic zebrafish

Cited by 103 publications

References 37 publications

Bioconcentration and metabolism of BDE-209 in the presence of titanium dioxide nanoparticles and impact on the thyroid endocrine system and neuronal development in zebrafish larvae

Bioconcentration and metabolism of BDE-209 in the presence of titanium dioxide nanoparticles and impact on the thyroid endocrine system and neuronal development in zebrafish larvae

Acute exposure to DE‐71: Effects on locomotor behavior and developmental neurotoxicity in zebrafish larvae

Prenatal Transfer of Polybrominated Diphenyl Ethers (PBDEs) Results in Developmental Neurotoxicity in Zebrafish Larvae

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