| Literature DB >> 28065758 |
K Dale1, J D Rasinger1, K L Thorstensen1, S Penglase1, S Ellingsen2.
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.Entities:
Keywords: Endosulfan; Neural development; Neurotoxicity; Vitamin E; Zebrafish
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Year: 2017 PMID: 28065758 DOI: 10.1016/j.fct.2017.01.004
Source DB: PubMed Journal: Food Chem Toxicol ISSN: 0278-6915 Impact factor: 6.023