Fin reduction is a novel and unexpected teratogenic effect of amikacin-treated zebrafish embryos

Abstract

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.

Keywords::

• Amikacin
• fin
• zebrafish
• ototoxicity
• neuromast