Tsai I-Ting, Chen Ying-Hsin, Chen Yau-Hung, Wang Yun-Hsin
Department of Chemistry, Tamkang University, 151, Yingzhuan Road, Danshui Dist., New Taipei City 25137, Taiwan, ROC.
J Toxicol Pathol. 2013 Mar;26(1):79-82. doi: 10.1293/tox.26.79. Epub 2013 Apr 22.
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.
尽管阿米卡星有医学用途，但对于其在斑马鱼中引起胚胎毒性（包括鳍减少）的潜在机制知之甚少。在本研究中，我们检测了经阿米卡星处理的斑马鱼胚胎中著名的自噬标志物mTOR（雷帕霉素靶蛋白）、atg10（自噬相关基因）、atg12和LC3（Atg8的哺乳动物同源物）的表达。我们的结果表明，与相应的模拟对照组相比，阿米卡星处理组中atg12的mRNA表达水平显著增加了1.5倍（p<0.05），而atg10和mTOR的表达水平分别显著降低了0.74倍（p<0.05）和0.58倍（p<0.05）。蛋白质免疫印迹分析显示，LC3蛋白表达由阿米卡星诱导。综上所述，这些数据表明阿米卡星诱导鳍减少是由鳍细胞自噬介导的。
