Immunofluorescence/fluorescence assessment of brain-derived neurotrophic factor, c-Fos activation, and apoptosis in the brain of zebrafish (Danio rerio) larvae exposed to glufosinate

Comaklı S., Kokturk M., Topal A., Ozkaraca M., Ceyhun S. B.

NeuroToxicology, cilt.69, ss.60-67, 2018 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 69
  • Basım Tarihi: 2018
  • Doi Numarası: 10.1016/j.neuro.2018.09.003
  • Dergi Adı: NeuroToxicology
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.60-67
  • Anahtar Kelimeler: c-FOS, BDNF, Zebrafish, Glufosinate, CELL-DEATH, IN-VIVO, CHITOSAN NANOPARTICLES, MOLECULAR-CLONING, GENE-EXPRESSION, MOUSE EMBRYOS, GROWTH-FACTOR, INDUCTION, TOXICITY, AMMONIUM
  • Atatürk Üniversitesi Adresli: Evet

Özet

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.