Amikacin-induced Fin Reduction is Mediated by Autophagy
- Authors
- Tsai, I.T., Chen, Y.H., Chen, Y.H., and Wang, Y.H.
- ID
- ZDB-PUB-130708-42
- Date
- 2013
- Source
- Journal of Toxicologic Pathology 26(1): 79-82 (Journal)
- Registered Authors
- Chen, Yau-Hung
- Keywords
- amikacin, autophagy, embryotoxicity, fin reduction, zebrafish
- MeSH Terms
- none
- PubMed
- 23723573 Full text @ J. Toxicol. Pathol.
Despite its medical use, little is known about the mechanisms underlying amikacin-induced embryotoxicity, including fin reduction, in zebrafish. In this study, we examined the expression of well-known autophagy markers mTOR (target of rapamycin), atg10 (autophagy-related gene), atg12 and LC3 (mammalian homolog of Atg8) in amikacin-treated zebrafish embryos. Our results indicated that the mRNA expression level of atg12 in the amikacin-treated group was significantly increased by 1.5-fold (p<0.05) compared with the corresponding mock control group, while the expression levels of atg10 and mTOR were significantly decreased by 0.74-fold (p<0.05) and 0.58-fold (p<0.05), respectively. Western blot analysis revealed that LC3 protein expression was induced by amikacin. Taken together, these data suggest that amikacin-induced fin reduction is mediated by fin cell autophagy.