PUBLICATION
Developmental toxicity and angiogenic defects of etoxazole exposed zebrafish (Danio rerio) larvae
- Authors
- Park, H., Lee, J.Y., Park, S., Song, G., Lim, W.
- ID
- ZDB-PUB-191022-35
- Date
- 2019
- Source
- Aquatic toxicology (Amsterdam, Netherlands) 217: 105324 (Journal)
- Registered Authors
- Keywords
- Angiogenesis, Development, Embryotoxicity, Etoxazole, Zebrafish
- MeSH Terms
-
- Animals
- Apoptosis/drug effects
- Cell Cycle/drug effects
- Cell Cycle/genetics
- Embryo, Nonmammalian/drug effects
- Embryo, Nonmammalian/metabolism
- Embryonic Development/drug effects
- Environmental Exposure*
- Humans
- Larva/drug effects
- Neovascularization, Pathologic/pathology*
- Oxazoles/toxicity*
- Reactive Oxygen Species/metabolism
- Toxicity Tests*
- Water Pollutants, Chemical/toxicity
- Zebrafish/embryology
- Zebrafish/physiology*
- PubMed
- 31634662 Full text @ Aquat. Toxicol.
Citation
Park, H., Lee, J.Y., Park, S., Song, G., Lim, W. (2019) Developmental toxicity and angiogenic defects of etoxazole exposed zebrafish (Danio rerio) larvae. Aquatic toxicology (Amsterdam, Netherlands). 217:105324.
Abstract
Etoxazole, a chitin synthesis inhibitor, is widely used to control insects and mites by causing developmental defects. Despite the many advantages of pesticides, the inhibitory effects of most pesticides including etoxazole are based on biochemical reaction and their widespread application is considered as a major risk to human health and the environment because of bioaccumulation and non-target toxic effects. Though used in agricultural area, the pesticide residues run off through rivers or ocean, where diverse aquatic organisms live. Since there are no studies evaluating the risks of etoxazole exposure in embryogenesis of aquatic organisms, we investigated the adverse effects of etoxazole on development and angiogenesis in zebrafish embryos, which are considered to be an effective model for detecting ecotoxicological effects of widely used compounds, especially affecting aquatic organisms. Etoxazole induced yolk sac and heart edema, as well as loss of viability, abnormal heart rate, and developmental deficiency. Through a mechanistic approach, we also showed that etoxazole caused reactive oxygen species accumulation, inhibited the expression of cell cycle activating genes, and induced apoptosis. In addition, we investigated effects of etoxazole on cardiovascular development by demonstrating the loss of vascular structure in response to etoxazole exposure in fli1:eGFP transgenic zebrafish model. Collectively, this first assessment demonstrating the effects of etoxazole on embryogenesis and cardiovascular development provides clear evidence for the toxicity of etoxazole and contributes important data towards formulating safety guidelines on the potential hazards of etoxazole for aquatic environment.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping