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

• Published in: Toxicology mechanisms and methods Vol. 22; no. 2; pp. 151 - 158
• Main Authors: Chen, Ying-Hsin, Tsai, I-Ting, Wen, Chi-Chung, Wang, Yun-Hsin, Cheng, Chien-Chung, Hu, Sheng-Chuan, Chen, Yau-Hung
• Format: Journal Article
• Language: English
• Published: England Informa Healthcare 01.02.2012; Taylor & Francis
• Subjects: Abnormalities, Drug-Induced - etiology; Amikacin; Amikacin - toxicity; Animal Fins - abnormalities; Animals; Anti-Bacterial Agents - toxicity; Apoptosis - drug effects; Danio rerio; Dose-Response Relationship, Drug; Embryo, Nonmammalian - drug effects; fin; Freshwater; neuromast; ototoxicity; Zebrafish
• ISSN: 1537-6516; 1537-6524
• DOI: 10.3109/15376516.2011.610385

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.