PUBLICATION
Bisphenol F causes disruption of gonadotropin-releasing hormone neural development in zebrafish via an estrogenic mechanism
- Authors
- Weiler, K., Ramakrishnan, S.
- ID
- ZDB-PUB-181207-30
- Date
- 2018
- Source
- Neurotoxicology 71: 31-38 (Journal)
- Registered Authors
- Keywords
- Bisphenol F, GnRH, development, endocrine disruption, estradiol, zebrafish
- MeSH Terms
-
- Animals
- Animals, Genetically Modified
- Benzhydryl Compounds/toxicity*
- Embryo, Nonmammalian/drug effects
- Embryonic Development/drug effects*
- Endocrine Disruptors/toxicity*
- Estradiol/administration & dosage
- Estradiol/physiology*
- Female
- Gonadotropin-Releasing Hormone/physiology*
- Male
- Neurons/drug effects*
- Neurons/pathology
- Neurons/physiology
- Phenols/toxicity*
- Pyrrolidonecarboxylic Acid/analogs & derivatives*
- Zebrafish
- Zebrafish Proteins/physiology
- PubMed
- 30521821 Full text @ Neurotoxicology
Citation
Weiler, K., Ramakrishnan, S. (2018) Bisphenol F causes disruption of gonadotropin-releasing hormone neural development in zebrafish via an estrogenic mechanism. Neurotoxicology. 71:31-38.
Abstract
Gonadotropin releasing hormone (GnRH) neurons in the brain are the main controllers of reproduction and reproductive behavior in most vertebrates, and are susceptible to endocrine disruption by different bisphenols. While the endocrine disrupting properties of bisphenol A have been well documented, commonly used analogues such as bisphenol F (BPF) are not as well studied. In this study we examined the effects of early, low-dose, chronic BPF exposure on the development of the GnRH neural system in the zebrafish embryo. Using a transgenic zebrafish model system with GnRH3 neurons tagged with green fluorescent protein (GFP), developing GnRH neurons in both the terminal nerve (TN) and preoptic area (POA) were observed. These are neuronal populations with the former associated with allied reproductive behaviors and the latter associated with pituitary-gonadal axis control. Embryos were exposed in vitro to 0.25, 0.5 and 1 μM BPF from fertilization to 3 days post fertilization (dpf). At 0.25 μM BPF exposure, both POA- and TN- GnRH3 neurons showed significant reductions in neural area at 2 dpf that did not persist to 3 dpf. The higher BPF doses did not show neuron size differences at 2 dpf, but showed reduction in TN-GnRH3 neuron area at 3 dpf. These effects of BPF were closely mimicked by different doses of estradiol. An estrogen antagonist, ICI, mitigated BPF effects on the embryo. This is the first study to show that BPF affects the developing GnRH neural system via an estrogen-mediated pathway.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping