PUBLICATION
Immunofluorescence/fluorescence assessment of brain-derived neurotrophic factor, c-Fos activation, and apoptosis in the brain of zebrafish (Danio rerio) larvae exposed to glufosinate
- Authors
- Çomakli, S., Köktürk, M., Topal, A., Özkaraca, M., Ceyhun, S.B.
- ID
- ZDB-PUB-180918-9
- Date
- 2018
- Source
- Neurotoxicology 69: 60-67 (Journal)
- Registered Authors
- Keywords
- BDNF, c-FOS, glufosinate, zebrafish
- MeSH Terms
-
- Aminobutyrates/toxicity*
- Animals
- Apoptosis/drug effects
- Apoptosis/physiology*
- Brain/drug effects
- Brain/metabolism*
- Brain-Derived Neurotrophic Factor/analysis
- Brain-Derived Neurotrophic Factor/metabolism*
- Dose-Response Relationship, Drug
- Female
- Fluorescent Antibody Technique
- Herbicides/toxicity
- Larva/drug effects
- Larva/metabolism*
- Male
- Proto-Oncogene Proteins c-fos/analysis
- Proto-Oncogene Proteins c-fos/metabolism*
- Random Allocation
- Survival Rate/trends
- Zebrafish
- PubMed
- 30222997 Full text @ Neurotoxicology
Citation
Çomakli, S., Köktürk, M., Topal, A., Özkaraca, M., Ceyhun, S.B. (2018) Immunofluorescence/fluorescence assessment of brain-derived neurotrophic factor, c-Fos activation, and apoptosis in the brain of zebrafish (Danio rerio) larvae exposed to glufosinate. Neurotoxicology. 69:60-67.
Abstract
In this study, we investigated the potential neuro-toxicological mechanism of the glufosinate in the brain of zebrafish larvae in terms of BDNF and c-Fos proteins by evaluating apoptosis, immunofluorescence BDNF, and c-FOS activation. We also measured survival rate, hatching rate, and body malformations during 96 h exposure time. For this purpose, zebrafish embryos were treated with graded concentrations of dosing solutions (0.5, 1, 3, and 5 ppm) of glufosinate. End of the treatment, acridine orange staining was used to detect apoptotic cells in the brain of zebrafish larvae at 96 hpf. Texas Red and FITC/GFP labeled protein-specific antibodies were used in immunofluorescence assay for BDNF and c-FOS, respectively. The results have indicated that exposure to glufosinate caused to embryonic death, hatching delay, induction of apoptosis, increasing of c-FOS activity and the level of BDNF in a dose-dependent manner. As a conclusion, we suggested that c-Fos might play a role in the regulation of BDNF which responses to prevent the cell from apoptosis even in case of unsuccessful in zebrafish larvae exposed to glufosinate.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping