PUBLICATION
Vitamin E reduces endosulfan-induced toxic effects on morphology and behavior in early development of zebrafish (Danio rerio)
- Authors
- Dale, K., Rasinger, J.D., Thorstensen, K.L., Penglase, S., Ellingsen, S.
- ID
- ZDB-PUB-170110-7
- Date
- 2017
- Source
- Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association 101: 84-93 (Journal)
- Registered Authors
- Ellingsen, Ståle
- Keywords
- Endosulfan, Neural development, Neurotoxicity, Vitamin E, Zebrafish
- MeSH Terms
-
- Animals
- Antioxidants/pharmacology*
- Behavior, Animal/drug effects*
- Embryo, Nonmammalian/drug effects*
- Embryo, Nonmammalian/pathology
- Endosulfan/toxicity*
- Insecticides/toxicity
- Oxidative Stress/drug effects
- Vitamin E/pharmacology*
- Zebrafish/growth & development*
- PubMed
- 28065758 Full text @ Food Chem. Toxicol.
- CTD
- 28065758
Citation
Dale, K., Rasinger, J.D., Thorstensen, K.L., Penglase, S., Ellingsen, S. (2017) Vitamin E reduces endosulfan-induced toxic effects on morphology and behavior in early development of zebrafish (Danio rerio). Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association. 101:84-93.
Abstract
The aim of this study was to investigate if vitamin E (α-TOC) modulates the developmental toxicity of the pesticide endosulfan (ESF), using a modified zebrafish embryotoxicity test (ZET). Zebrafish (Danio rerio) embryos were exposed from 6 to 72 h post fertilization (hpf) to either ESF (0.1-50 mg/L) or α-TOC (0.01-3 mM) alone or in combination. The effects of these exposures on embryonic morphology, larval behavior and antioxidant gene expression were analyzed. Phenotypic analysis at 48 hpf showed that ESF led to a dose-dependent increase in embryonic deformities, including axis malformations, pericardial edema and reduced pigmentation. Co-exposure of ESF with α-TOC (1-3 mM) significantly (p < 0.05) reduced ESF-induced embryonic malformations. Exposure to solely α-TOC did not affect rates of survival or malformations. Behavior studies showed that ESF caused hyperactivity at 5 days post fertilization, indicating a developmental neurotoxic effect. The ESF-induced hyperactivity was ameliorated by α-TOC. Elevated ESF concentrations caused down-regulation of the antioxidant genes cuzn-sod, gpx1a and cat, suggesting that ESF promoted oxidative stress in the embryos. α-TOC did not prevent the ESF-induced dysregulation of these genes. These results demonstrate that α-TOC protects against phenotypic and behavioral effects caused by ESF but did not rescue ESF-induced aberrations in antioxidant gene expression.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping