ZFIN ID: ZDB-PUB-120117-14
Fin reduction is a novel and unexpected teratogenic effect of amikacin-treated zebrafish embryos
Chen, Y.H., Tsai, I.T., Wen, C.C., Wang, Y.H., Cheng, C.C., Hu, S.C., and Chen, Y.H.
Date: 2012
Source: Toxicology mechanisms and methods   22(2): 151-158 (Journal)
Registered Authors: Chen, Yau-Hung
Keywords: Amikacin, fin, zebrafish, ototoxicity, neuromast
MeSH Terms:
  • Abnormalities, Drug-Induced/etiology*
  • Amikacin/toxicity*
  • Animal Fins/abnormalities*
  • Animals
  • Anti-Bacterial Agents/toxicity*
  • Apoptosis/drug effects
  • Dose-Response Relationship, Drug
  • Embryo, Nonmammalian/drug effects
  • Zebrafish
PubMed: 22242631 Full text @ Toxicol. Mech. Methods

We used zebrafish as a model to assess amikacin-induced embryotoxicity. We exposed zebrafish embryos to amikacin, using different amikacin doses (0–10 ppm), durations (12–48 h), and onsets (0, 24, 48 hpf). Amikacin-induced embryonic toxicity and reduced survival rate were found dependent on the exposure dose, duration and onset. Based on immunostaining with neuron-specific antibodies, amikacin reduced the number and size of zebrafish neuromasts. In addition, Amikacin caused pelvic, dorsal and anal fin defects in dose-dependent and duration-dependent manners. Proliferating cell nuclear antigen immunostaining revealed that amikacin-induced fin defects were not due to reduction of proliferating mesenchymal cells. TUNEL assay demonstrated that amikacin-induced fin defects might not associate with apoptosis. Therefore, further investigations are required to elucidate if other cell death pathways are involved in amikacin-induced fin defects.