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首页> 外文期刊>Journal of applied toxicology >Developmental toxicity of auranofin in zebrafish embryos
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Developmental toxicity of auranofin in zebrafish embryos

机译：斑马鱼胚胎中Auranofin的发育毒性

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Auranofin (AF) is used in clinic for the treatment of rheumatoid arthritis, repurposing of AF as an anticancer drug has just finished a phase I/II clinical trial, but the developmental toxicity of AF remains obscure. This study focused on its developmental toxicity by using zebrafish embryos. Zebrafish embryos were exposed to different concentrations (1, 2.5, 5, 10m) of AF from 2h post-fertilization (hpf) to 72 hpf. At 72 hpf, two major developmental defects caused by AF were found, namely severe pericardial edema and hypopigmentation, when embryos were exposed to concentrations higher than 2.5m. Biochemical detection of oxidative stress enzyme combined with expressions of a series of genes related to oxidative stress, cardiac, metal stress and pigment formation were subsequently tested. The superoxide dismutase activity was decreased while malondialdehyde content was accumulated by AF treatment. The expression of oxidative stress-related genes (sod1, gpx1a, gst), pigment-related genes (mitfb, trp-1a) and one metal stress-related gene ctr1 were all decreased by AF exposure. The expressions of cardiac-related genes (amhc, vmhc) and one metal-related gene hsp70 were found to be significantly upregulated by AF exposure. These findings indicated the potential developmental toxicity of AF on zebrafish early development. Copyright (C) 2016 John Wiley & Sons, Ltd.
机译：Auranofin（AF）用于治疗类风湿性关节炎的临床，作为抗癌药物的重新施用刚刚完成了I / II期临床试验，但AF的发育毒性仍然模糊不清。本研究专注于使用斑马鱼胚胎的发育毒性。将斑马鱼胚胎暴露于从施用后2小时（HPF）至72 HPF的2小时的不同浓度（1,2.5,5,100m）的AF。在72 HPF下，发现AF引起的两种主要发育缺陷，即严重的心包水肿和低次成像，当胚胎暴露于高于2.5M的浓度时。随后测试了氧化应激酶的生化检测与氧化应激，心脏，金属应激和颜料形成相关的一系列基因的表达。超氧化物歧化酶活性减少，而AF治疗累积丙二醛含量。 AF暴露，氧化应激相关基因（SOD1，GPX1A，GST），颜料相关基因（MITFB，TRP-1A）和一种金属应激相关基因CTR1全部降低。发现心脏相关基因（AMHC，VMHC）和一种金属相关基因HSP70的表达被AF暴露显着上调。这些发现表明了AF对斑马鱼早期发展的潜在发育毒性。版权所有（c）2016 John Wiley＆Sons，Ltd。

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