PUBLICATION
Modulation by ellagic acid of DCA-induced developmental toxicity in the zebrafish (Danio rerio)
- Authors
- Williams, F.E., Sickelbaugh, T.J., and Hassoun, E.
- ID
- ZDB-PUB-060816-31
- Date
- 2006
- Source
- Journal of biochemical and molecular toxicology 20(4): 183-190 (Journal)
- Registered Authors
- Williams, Fred
- Keywords
- Zebrafish, Embryos, Danio rerio, Dichloroacetate, Malformations, Reactive Oxygen Species, Ellagic Acid, Drinking Water Disinfection By-products
- MeSH Terms
-
- Animals
- Dichloroacetic Acid/toxicity*
- Ellagic Acid/pharmacology*
- Embryo, Nonmammalian/drug effects
- Embryo, Nonmammalian/embryology
- Embryo, Nonmammalian/metabolism
- Heart Rate/drug effects
- Nitric Oxide/biosynthesis
- Superoxides/metabolism
- Zebrafish/embryology*
- Zebrafish/growth & development*
- Zebrafish/metabolism
- PubMed
- 16906523 Full text @ J. Biochem. Mol. Toxicol.
Citation
Williams, F.E., Sickelbaugh, T.J., and Hassoun, E. (2006) Modulation by ellagic acid of DCA-induced developmental toxicity in the zebrafish (Danio rerio). Journal of biochemical and molecular toxicology. 20(4):183-190.
Abstract
The ability of ellagic acid (EA) to modulate dichloroacetic acid (DCA)-induced developmental toxicity and oxidative damage was examined in zebrafish embryos. Embryos were exposed to 20 mM EA administered concomitantly with 32 mM DCA at 4 hours postfertilization (hpf) and 20 h later. Embryos were observed through 144 hpf for developmental malformations, and production of superoxide anion (SA) and nitric oxide (NO) was determined in embryonic homogenates. DCA was shown to produce developmental abnormalities and significant levels of SA and NO in zebrafish embryos. EA exposure alleviated the developmental malformations observed in treated embryos and decreased the levels of SA and NO in those same embryos. Less than 10% of DCA + EA exposed embryos showed developmental malformations compared to 100% of embryos treated with DCA alone. Animals in this group that developed malformations were shown to have fewer defects than those treated with DCA only. Taken together, the results confirm the involvement of oxidative stress in the developmental toxicity of DCA in zebrafish embryos, and suggest possible protection against those effects with the use of antioxidants.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping