PUBLICATION
Developmental toxicity of endocrine disruptors in early life stages of zebrafish, a genetic and embryogenesis study
- Authors
- Santos, D., Matos, M., Coimbra, A.M.
- ID
- ZDB-PUB-140831-3
- Date
- 2014
- Source
- Neurotoxicology and teratology 46: 18-25 (Journal)
- Registered Authors
- Keywords
- 17α-ethinylestradiol, embryo-larval development, fadrozole, gene expression, genistein, zebrafish
- MeSH Terms
-
- Animals
- Apoptosis/drug effects
- Apoptosis/genetics
- Endocrine Disruptors/administration & dosage*
- Endocrine Disruptors/toxicity*
- Fadrozole/administration & dosage
- Fadrozole/toxicity
- Fish Proteins/drug effects*
- Fish Proteins/genetics*
- Gene Expression/drug effects
- Genistein/administration & dosage
- Genistein/toxicity
- Heart Rate/drug effects
- Proto-Oncogene Proteins c-jun/genetics
- Receptors, Androgen/genetics
- Receptors, Estrogen/genetics
- Somites/drug effects
- Somites/embryology
- Tumor Suppressor Protein p53/genetics
- Zebrafish/embryology*
- Zebrafish/genetics*
- Zebrafish Proteins/genetics
- PubMed
- 25172296 Full text @ Neurotoxicol. Teratol.
Citation
Santos, D., Matos, M., Coimbra, A.M. (2014) Developmental toxicity of endocrine disruptors in early life stages of zebrafish, a genetic and embryogenesis study. Neurotoxicology and teratology. 46:18-25.
Abstract
Endocrine disrupting compounds (EDCs) are capable of interfering with the endocrine system and are increasingly widespread in the aquatic environments. In the present study, zebrafish (Danio rerio) embryos and larvae were used to assess how EDCs may interfere with embryogenesis. Therefore, zebrafish embryos were exposed to 17α-ethinylestradiol (EE2: 0.4, 2, 4 and 20ng/L), genistein (Gen: 2, 20, 200 and 2000ng/L) and fadrozole (Fad: 2, 10, 50 and 250μg/L), between 2 and 144h post-fertilization (hpf). Somite development, heartbeat, malformations, mortality and hatching rates were evaluated. In parallel, the expression patterns of hormone receptors (esr1, esr2a, esr2b and ar) and apoptotic pathways related genes (p53 and c-jun) were determined using quantitative real-time PCR. Results showed that EE2, Gen and Fad caused a higher mortality and also malformations in larvae compared with control. A significant toxic effect was observed in the heartbeat rate, at 144 hpf, in larvae exposed to EE2 and Fad. QPCR revealed alterations in the expression levels of all the evaluated genes, at different time points. esr1 and c-jun genes were upregulated by EE2 and Gen exposure while the expression of esr2a, esr2b and ar genes were down-regulated. Fad exposure decreased esr1, p53 and c-jun expression levels. This study shows a toxic effect of EE2, Gen and Fad to vertebrate embryogenesis and a relation between hormones action and apoptosis pathways.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping