PUBLICATION
Developmental toxicity and alteration of gene expression in zebrafish embryo exposed to 6-benzylaminopurine
- Authors
- Wang, W., Wang, B., Liu, Z., Xia, X.
- ID
- ZDB-PUB-190610-3
- Date
- 2019
- Source
- Chemosphere 233: 336-346 (Journal)
- Registered Authors
- Keywords
- 6-Benzylaminopurine (6-BA), Cardiac toxicity, Developmental toxicity, Teratogenic effect, Zebrafish
- MeSH Terms
-
- Animals
- Apoptosis/drug effects
- Apoptosis/genetics
- Benzyl Compounds/administration & dosage
- Benzyl Compounds/toxicity*
- Dose-Response Relationship, Drug
- Embryo, Nonmammalian/drug effects*
- Embryo, Nonmammalian/pathology
- Female
- Gene Expression Regulation, Developmental/drug effects*
- Humans
- Male
- Purines/administration & dosage
- Purines/toxicity*
- Toxicity Tests, Acute
- Zebrafish/embryology*
- PubMed
- 31176896 Full text @ Chemosphere
Citation
Wang, W., Wang, B., Liu, Z., Xia, X. (2019) Developmental toxicity and alteration of gene expression in zebrafish embryo exposed to 6-benzylaminopurine. Chemosphere. 233:336-346.
Abstract
6-benzylaminopurine (6-BA) is widely used in agriculture and horticulture as plant growth regulator. Its excessive use may pose a potential risk to both environment and human health, which is causing great concern. This study was undertaken to assess the acute developmental toxicity of 6-BA to zebrafish embryos based on OECD protocols and mortality, hatching rate and malformation were investigated. Results showed that the 96 h-LC50 and 96 h- EC50 values were 63.29 mg/L and 41.86 mg/L, respectively. No mortality or teratogenic effects were found at concentrations lower than 10 mg/L 6-BA at concentrations higher than 50 mg/L significantly inhibited hatchability and embryo development, induced serious toxicity characterized by morphologic abnormalities (elongated pericardium, heart and yolk sac edema, spine curvature) and functional failure (slow spontaneous movement and heart rate, growth retardation, yolk sac absorption retention). Moreover, 6-BA-induced apoptosis was observed in embryos by the acridine orange staining and confirmed by the apoptotic-related genes, all of which p53 was significantly up-regulated at concentrations higher than 10 mg/L, bax at concentrations higher than 12.5 mg/L, while bcl2 was down-regulated at concentrations higher than 25 mg/L. As for genes of cardiac development, qPCR results demonstrated that nkx2.5, gata5, and amhc were significantly down-regulated at concentrations higher than 25 mg/L, vmhc and atp2a2a at concentration of 50 mg/L, in contrast, hand2 was up-regulated at concentration of 50 mg/L. Our data indicate that 6-BA induces a dose-dependent toxicity resulting in apoptosis through the involvement of p53-dependent pathways and hindering normal heart development in zebrafish embryos.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping