马兜铃酸对斑马鱼胚胎肾毒性作用

选用肾发育完成(受精后3天)的斑马鱼(Danio rerio)胚胎,用马兜铃酸进行染毒处理,观察胚胎的表型变化及死亡情况,分析马兜铃酸对胚胎的毒性作用及规律;利用肾荧光观察及肾组织切片,观察马兜铃酸处理后胚胎肾形态和肾组织结构的改变情况;利用qPCR检测马兜铃酸处理前后nephrin的表达变化,初步探讨足细胞在马兜铃酸毒性作用中的功能状态。20μmol/L马兜铃酸处理24 h后,胚胎出现明显眼周水肿表现;在马兜铃酸高浓度组(40~80μmol/L),除眼周水肿外,胚胎血循环系统功能出现异常,表现为心率降低、血流缓慢甚至停滞;荧光显微镜下观察发现,马兜铃酸处理组胚胎肾出现肾小球囊性膨胀、前肾管囊性扩张和形态异常;切片显示马兜铃酸处理组胚胎肾组织结构受到损害,表现为肾小球结构疏松、囊性扩张,前肾管上皮细胞细胞排列松散、紊乱及管腔扩张样改变;qPCR结果,马兜铃酸处理组斑马鱼胚胎nephrin的表达水平比对照组显著降低(P0.01)。研究表明,马兜铃酸能损害斑马鱼胚胎肾结构和功能,其毒性作用与肾小球足细胞的功能改变有关。     

迷迭香酸对硫酸铜致斑马鱼胚胎毒性的抑制作用

本文探讨硫酸铜(CuSO_4)对斑马鱼(Danio rerio)胚胎发育的毒性效应,使用迷迭香酸(RA)抑制CuSO_4对斑马鱼胚胎发育的毒性并探讨其作用机制。收集受精后1 h(1 hpf)的斑马鱼胚胎暴露于不同浓度的CuSO_4溶液,或含有不同浓度迷迭香酸的CuSO_4溶液,对照组培养在E3培养液中,观察胚胎死亡、孵化及畸形情况,计算胚胎死亡率、孵化率和畸形率;以活性氧(ROS)荧光探针DCFH-DA染色法检测迷迭香酸保护下胚胎的活性氧水平。对实验数据进行方差分析。结果显示:(1)CuSO_4浓度超过一定量时能诱导斑马鱼胚胎死亡和畸形,胚胎孵化率也降低。CuSO_4对96 hpf斑马鱼胚胎的半致死浓度(LC50)为7.7μmol/L,半致畸浓度(EC50)为1.9μmol/L。(2)在96 hpf,迷迭香酸与8μmol/L CuSO_4共同处理组斑马鱼胚胎的死亡率明显降低,孵化率升高。迷迭香酸与1.6μmol/LCuSO_4共同处理组斑马鱼胚胎的畸形率降低。(3)CuSO_4单独处理组的活性氧含量明显高于迷迭香酸与CuSO_4共同处理组和对照组。结果表明,CuSO_4暴露对斑马鱼胚胎发育的毒性效应可能与活性氧升高导致的氧化应激相关;迷迭香酸抑制CuSO_4对斑马鱼胚胎发育的毒性作用,可能与减少活性氧生成有关。     

卡培他滨对非靶标生物斑马鱼胚胎的发育毒性研究

为评价抗肿瘤药物卡培他滨(CAP)对非靶标生物的毒性, 以斑马鱼胚胎为受试生物, 研究了CAP对斑马鱼胚胎的发育毒性及对其抗氧化酶系的影响。结果表明, 直接暴露于卡培他滨中, 造成斑马鱼胚胎死亡率和畸形率增加, 且其机能有所下降。当暴露浓度高于20 μg·L-1时, 处理后的斑马鱼胚胎死亡率和畸形率显著升高, 与对照组相比有极显著差异。CAP浓度为0.2 μg·L-1时, 超氧化物歧化酶 (SOD) 活性和过氧化氢酶 (CAT) 活性均显著升高, 表明机体遭受一定程度的氧化损伤; 当浓度高于20 μg·L-1时, SOD和CAT活性显著降低, 表明斑马鱼仔鱼所受氧化损伤超出其自我修复能力, 引发致死性伤害。本文从发育毒性及氧化应激着手, 探究了CAP对非靶标生物的潜在危害, 为其生态效应提供一定的科学依据。     

产紫青霉突变菌株Li-3-9的发酵条件优化及红色素安全性评价

本实验对前期研究得到的具有高产红色素能力的产紫青霉突变菌株Penicillium purpurogenum Li-3-9的发酵条件进行优化的同时作出了对红色素的安全性评价。在单因素试验的基础上,采用Box-Behnken试验设计优化了蔗糖浓度、酵母膏浓度和装液量对红色素色价的影响;并且研究了P. purpurogenum Li-3-9产生的红色素对斑马鱼胚胎的毒性效应。结果表明,最佳发酵条件为：蔗糖40g/L、酵母膏4g/L、装液量为45mL、接种量4%、培养温度32℃、初始pH值6.9、培养时间168h、摇床转速150r/min,红色素色价最高达到了11.4U/mL。通过计算斑马鱼胚胎致死率、心率、畸形率及孵化率可知,该色素无致死毒性,并且对斑马鱼胚胎发育具有一定的促进作用。     

视黄酸缺乏对斑马鱼心脏房室分化的影响

目的 通过化学遗传学方法建立视黄酸缺乏的斑马鱼模型,探讨视黄酸缺乏对斑马鱼胚胎心脏前后轴发育即房室分化的影响.方法 在斑马鱼胚胎孵育的5 hpf,用不同浓度梯度的视黄醛脱氢酶2抑制剂DEAB(1×10-6、5×10-6、10×10-6、25×10-6 mol/L)处理斑马鱼胚胎,实时观察斑马鱼胚胎发育的全过程.通过给予斑马鱼胚胎外源性视黄酸,观察其对DEAB的拮抗作用.应用胚胎整体原位杂交观察视黄酸缺乏对心脏特异基因vmhc和amhc表达的影响.结果 斑马鱼胚胎的生存率随着DEAB处理浓度的增加而降低,当DEAB浓度≥5×10-6 mol/L时,斑马鱼的畸胎率达100%.5×10-6 mol/L DEAB的致畸作用能够被1×10-9mol/L外源性视黄酸所拮抗.整体原位杂交结果显示视黄酸缺乏会导致斑马鱼胚胎心脏房室分化异常,表现为vmhc表达细胞的范围增大,amhc表达细胞的范围缩小.结论 通过外源性DEAB处理能有效地建立视黄酸缺乏的斑马鱼模型,DEAB影响胚胎发育存在剂量依赖性.视黄酸在斑马鱼心脏前后轴发育过程中起重要调控作用,心脏发育早期视黄酸缺乏会抑制心房的发育而支持心室的发育,出现房室分化异常.     

香附水提液对小麦幼苗生理活性酶的影响

鉴于中草药在抗菌、杀菌,抑制细胞分裂等方面的作用,利用中草药来抑制小麦穗发芽或许是一种新的途径和方法。为了初步研究香附水提液在小麦种子萌发过程中对幼苗生理活性酶的影响,采用室内培养皿培养法,分析不同浓度的香附水提液浸种后对小麦幼苗的α-淀粉酶含量、叶绿素含量和过氧化氢酶活性的作用,结果表明α-淀粉酶含量、叶绿素含量随水提液浓度的增加而降低,过氧化氢酶活性含量则随之递增,并且以香附水提液浓度为120 g/L和150 g/L的处理差异显著,此为研究开发抑制小麦穗发芽的中草药生物抑制剂提供试验依据。     

诺氟沙星对斑马鱼胚胎发育的毒性作用及对TGF-β1的影响

旨在通过观察不同浓度诺氟沙星对斑马鱼胚胎不同发育时期的毒性作用,以及对TGF-β1基因表达的影响。配制诺氟沙星浓度为0、10、20、40μmol/L,将斑马鱼胚胎暴露在上述浓度的诺氟沙星中。观察在胚胎不同发育时期,诺氟沙星对斑马鱼脊柱弯曲、心包囊肿、卵黄囊肿和死亡率的影响,以及使用实时定量聚合酶链式反应(q PCR)检测其对TGF-β1基因表达的影响。结果显示,诺氟沙星对斑马鱼的胚胎发育有明显影响,主要表现在脊柱弯曲、心包囊肿和卵黄囊肿,随着诺氟沙星暴露浓度的增大,胚胎的发育延迟,孵化时间延长,胚胎死亡率增加;当诺氟沙星暴露浓度为40μmol/L时,96 hpf的胚胎死亡率达到76.45%;与正常状态相比,暴露于不同浓度诺氟沙星的斑马鱼胚胎中TGF-β1基因的m RNA表达随发育时间延长而增加趋势减缓。说明诺氟沙星对斑马鱼胚胎发育的致畸作用与致死作用有显著的影响。提示水体中残留的诺氟沙星对鱼类的生殖与发育具有潜在的危害。     

新疆不同地区产蜂胶抗氧化活性研究

测定新疆不同地区产蜂胶总黄酮含量,并通过DPPH-体系、羟基自由基体系、超氧阴离子自由基体系对蜂胶醇提物抗氧化活性进行研究,与槲皮素进行比较.结果表明:新疆伊犁那拉提、尼勒克县产蜂胶总黄酮含量分别为9.015 ±0.203％、7.710±0.259％无显著差异(P＞0.05).那拉提、尼勒克县产蜂胶醇提物浓度100μ,g/mL时对超氧阴离子清除活性与槲皮素比较没有显著差异(P＞0.05),那拉提、尼勒克县产蜂胶醇提物IC50为46.48、47.19 μg/mL,槲皮素IC50为21.26 μg/mL;当那拉提、尼勒克县产蜂胶醇提物浓度为100、80 μg/mL时对羟基自由基的清除活性与槲皮素比较没有显著差异(P＞0.05),那拉提、尼勒克县产蜂胶醇提物IC50为37.54、36.24 μg/mL,槲皮素IC50为28.18 μg/mL;浓度为40 μg/mL时那拉提蜂胶醇提物对DPPH自由基清除活性与槲皮素进行比较,没有显著差异(P＞0.05),那拉提、尼勒克县产蜂胶醇提物IC50为18.37、20.12μg/mL,槲皮素IC50为9.95 μg/mL,表明蜂胶是一种天然有效的自由基清除剂.     

外源性视黄酸对斑马鱼心血管系统发育的影响

目的观察不同浓度外源性视黄酸对斑马鱼早期胚胎和心血管系统发育的影响,为进一步研究视黄酸影响斑马鱼心脏前后轴(A-P轴)发育的分子机制提供形态学依据。方法选择斑马鱼胚胎孵育的3,6,9·5,12h四个时间点,用不同浓度视黄酸(1×10-6,1×10-7,4×10-8,1×10-8mol/L)处理斑马鱼胚胎,在解剖显微镜下实时观察斑马鱼胚胎心脏发育的全过程和视黄酸对斑马鱼心脏发育的影响。并采用胚胎整体原位杂交技术观察flk-1mRNA在斑马鱼胚胎的表达。结果1×10-6mol/L视黄酸可导致斑马鱼胚胎表现出多系统的严重畸形,胚胎很快死亡。在胚胎孵育的9·5、12h给与10-7~10-8mol/L浓度的视黄酸,胚胎只表现出心血管系统的畸形,其他系统无明显异常。胚胎整体原位杂交显示视黄酸对flk-1mRNA在斑马鱼胚胎血管的表达没有影响。结论视黄酸影响斑马鱼胚胎心脏发育有剂量依赖性和严格的时间窗,视黄酸影响心脏前后轴发育的关键时间是原肠胚晚期。视黄酸处理组胚胎的循环缺陷主要为心脏发育异常所致。10-7~10-8mol/L浓度视黄酸在9·5、12h处理斑马鱼胚胎可以作为研究心脏发育调控机制的动物模型。     

马兜铃酸对斑马鱼肾损伤因子（KIM-1）表达的影响

采用分子定量方法检测斑马鱼(Danio rerio)幼鱼组织中KIM-1蛋白含量和基因表达水平,了解马兜铃酸处理后斑马鱼体内肾损伤因子的表达变化情况,并与幼鱼表型变化相比较,探讨KIM-1作为肾功能特异标志物在斑马鱼肾功能损伤评价中的应用价值。结果显示,马兜铃酸处理30 h后,幼鱼出现水肿,水肿发生率呈剂量依赖性特点。0.5~5.0μmol/L马兜铃酸处理组幼鱼水肿发生率与对照组差异不明显,但幼鱼KIM-1因子的蛋白含量及Kim-1基因表达水平比正常对照组显著升高,在马兜铃酸浓度为2μmol/L时达到最高。表明在肾功能损伤检测中,KIM-1是一种比表型更早发生变化的指标。     

三氯乙烯对斑马鱼胚胎心脏发育的毒性作用及机制*

目的:研究三氯乙烯(TCE)对斑马鱼胚胎心脏发育的毒性作用及其机制,为寻找干预靶点提供实验依据。方法:斑马鱼胚胎来自于国家斑马鱼资源中心,分为DMSO组(对照组)、DMSO+CHIR组、DMSO+XAV组、TCE处理组、TCE+CHIR组和TCE+XAV组(TCE设置为1、10、100 ppb三个不同的浓度;DMSO:二甲基亚砜;CHIR:CHIR-99021,Wnt信号通路激活剂;XAV:XAV-939,Wnt信号通路抑制剂),每组60条。斑马鱼胚胎饲养于系统养殖水中,恒温28℃,每隔24 h更换养殖水,并分别加入相应药物。连续培养72 h,收集斑马鱼胚胎的心脏组织,提取RNA进行转录组芯片分析,并以荧光定量PCR验证Wnt信号通路相关基因的表达。结果:与对照组相比,三氯乙烯暴露导致斑马鱼心脏畸形显著增加,以心房心室比例异常、环化不全以及心包水肿等为主要表型。芯片分析结果显示,TCE处理组Wnt信号通路相关基因(Axin2、Sox9b、Nkx2.5)表达受到显著影响。qPCR结果进一步验证,TCE处理组与DMSO对照组相比,Wnt通路靶基因Axin2、Sox9b及Nkx2.5的mRNA水平显著下调(P＜0.05),提示Wnt信号通路被抑制。Wnt激活剂CHIR降低TCE导致的斑马鱼胚胎心脏发育异常,而添加Wnt通路抑制剂XAV后,斑马鱼胚胎心脏畸形率显著增加(P＜0.05)。结论:三氯乙烯暴露导致斑马鱼胚胎心脏畸形,Wnt信号通路参与三氯乙烯的心脏发育毒性。     

Antibiotic Toxicity and Absorption in Zebrafish Using Liquid Chromatography-Tandem Mass Spectrometry

Evaluation of drug toxicity is necessary for drug safety, but in vivo drug absorption is varied; therefore, a rapid, sensitive and reliable method for measuring drugs is needed. Zebrafish are acceptable drug toxicity screening models; we used these animals with a liquid chromatography-tandem mass spectrometry (LC-MS/MS) method in a multiple reaction monitoring mode to quantify drug uptake in zebrafish to better estimate drug toxicity. Analytes were recovered from zebrafish homogenate by collecting supernatant. Measurements were confirmed for drugs in the range of 10–1,000 ng/mL. Four antibiotics with different polarities were tested to explore any correlation of drug polarity, absorption, and toxicity. Zebrafish at 3 days post-fertilization (dpf) absorbed more drug than those at 6 h post-fertilization (hpf), and different developmental periods appeared to be differentially sensitive to the same compound. By observing abnormal embryos and LD₅₀ values, zebrafish embryos at 6 hpf were considered to be suitable for evaluating embryotoxicity. Also, larvae at 3 dpf were adapted to measure acute drug toxicity in adult mammals. Thus, we can exploit zebrafish to study drug toxicity and can reliably quantify drug uptake with LC-MS/MS. This approach will be helpful for future studies of toxicology in zebrafish.     

miR-22心肌特异转基因斑马鱼的构建及心肌肥厚的评估

目的:构建miR-22心肌特异转基因斑马鱼系,在体评估miR-22对于心肌肥厚的作用。方法:构建pTol2-CMLC2-miR-22-IRES-EGFP表达载体。通过显微注射的方法将tol2重组质粒于一细胞期注射入斑马鱼受精卵胚胎中,荧光筛选获得心肌特异表达绿色荧光的斑马鱼胚胎,并稳定表达传代。然后对稳定传代的成年斑马鱼心脏进行心肌肥厚及心功能的检测。结果:成功建立了miR-22心肌特异转基因斑马鱼系,通过定量PCR确定心肌中miR-22表达升高,荧光显微镜观察发现斑马鱼心肌出现绿色荧光。miR-22心脏特异过表达的转基因鱼系的成年鱼与野生对照组相比,出现了心肌肥厚的现象,心肌肥厚分子标志物nppa、myh7明显升高。斑马鱼心脏病理切片结果同样显示出miR-22心肌特异转基因斑马鱼出现了心肌肥厚的现象。结论:成功构建了miR-22心肌特异转基因斑马鱼,为研究心肌中miR-22的生物学功能提供了重要的工具,并证明miR-22心脏特异过表达会引起斑马鱼心肌肥厚。     

Optimisation of Embryonic and Larval ECG Measurement in Zebrafish for Quantifying the Effect of QT Prolonging Drugs

Effective chemical compound toxicity screening is of paramount importance for safe cardiac drug development. Using mammals in preliminary screening for detection of cardiac dysfunction by electrocardiography (ECG) is costly and requires a large number of animals. Alternatively, zebrafish embryos can be used as the ECG waveform is similar to mammals, a minimal amount of chemical is necessary for drug testing, while embryos are abundant, inexpensive and represent replacement in animal research with reduced bioethical concerns. We demonstrate here the utility of pre-feeding stage zebrafish larvae in detection of cardiac dysfunction by electrocardiography. We have optimised an ECG recording system by addressing key parameters such as the form of immobilization, recording temperature, electrode positioning and developmental age. Furthermore, analysis of 3 days post fertilization (dpf) zebrafish embryos treated with known QT prolonging drugs such as terfenadine, verapamil and haloperidol led to reproducible detection of QT prolongation as previously shown for adult zebrafish. In addition, calculation of Z-factor scores revealed that the assay was sensitive and specific enough to detect large drug-induced changes in QTc intervals. Thus, the ECG recording system is a useful drug-screening tool to detect alteration to cardiac cycle components and secondary effects such as heart block and arrhythmias in zebrafish larvae before free feeding stage, and thus provides a suitable replacement for mammalian experimentation.     

Lrrc10 is required for early heart development and function in zebrafish

Leucine-rich Repeat Containing protein 10 (LRRC10) has recently been identified as a cardiac-specific factor in mice. However, the function of this factor remains to be elucidated. In this study, we investigated the developmental roles of Lrrc10 using zebrafish as an animal model. Knockdown of Lrrc10 in zebrafish embryos (morphants) using morpholinos caused severe cardiac morphogenic defects including a cardiac looping failure accompanied by a large pericardial edema, and embryonic lethality between day 6 and 7 post fertilization. The Lrrc10 morphants exhibited cardiac functional defects as evidenced by a decrease in ejection fraction and cardiac output. Further investigations into the underlying mechanisms of the cardiac defects revealed that the number of cardiomyocyte was reduced in the morphants. Expression of two cardiac genes was deregulated in the morphants including an increase in atrial natriuretic factor, a hallmark for cardiac hypertrophy and failure, and a decrease in cardiac myosin light chain 2, an essential protein for cardiac contractility in zebrafish. Moreover, a reduced fluorescence intensity from NADH in the morphant heart was observed in live zebrafish embryos as compared to control. Taken together, the present study demonstrates that Lrrc10 is necessary for normal cardiac development and cardiac function in zebrafish embryos, which will enhance our understanding of congenital heart defects and heart disease.     

氯丙嗪在斑马鱼胚胎和早期幼鱼发育过程中的神经毒性作用

目的 采用模式动物斑马鱼作为研究对象,观察氯丙嗪（chlorpromazine,CPZ）暴露对胚胎和幼鱼早期神经发育的影响.方法 在一般毒性评价的基础上,通过整体胚胎细胞凋亡检测和脑组织病理学检查,了解CPZ对神经发育的器质性改变;采用神经行为学方法,包括幼鱼触动逃避反应、自发运动以及惊恐逃避反射等,研究氯丙嗪暴露所致的神经发育功能性障碍.结果斑马鱼胚胎受精后6 h（6 hpf）～72 hpf暴露于CPZ（≥5 mg/L）可引起胚胎和幼鱼死亡、致畸和幼鱼孵化延迟,并呈浓度和时间依赖性;采用吖啶橙染色检测36 hpf整体胚胎凋亡细胞,发现凋亡细胞主要集中在胚胎中脑、后脑、丘脑以及中后脑连接区、脊索和尾部等处;脑组织病理学检测发现,7dpf幼鱼颅腔增大、脑体积减小、脑细胞缩小且细胞间隙增宽.6～72 hpf CPZ（≥0.0625 mg/L）暴露后,幼鱼神经行为学研究发现,CPZ（≥0.125 mg/L）可引起3dpf幼鱼触觉运动能力下降;CPZ（≥0 5 mg/L）可浓度依赖性地抑制幼鱼自发运动,并出现僵直不动、震颤或快速刻板式转圈运动等行为改变;光惊恐实验中,暗环境下各暴露组幼鱼对突发强光刺激均表现为惊跳逃避,并且暗-光交替期运动加速度变化与对照组无显著差异;在撤除光源后,1mg/L和2 mg/L暴露组幼鱼暗适应时程缩短,而0.125 mg/L和0.25 mg/L暴露组暗适应时程延长,提示CPZ对外界刺激引发的幼鱼活跃游动有抑制和促进双重毒性作用.结论 CPZ暴露对斑马鱼胚胎和幼鱼具有明显的神经发育毒性作用.模式动物斑马鱼作为一种高通量筛选模型在外源性化合物神经发育毒性评价中具有较好的应用前景.     

Modulation by ellagic acid of DCA-induced developmental toxicity in the zebrafish (Danio rerio)

The ability of ellagic acid (EA) to modulate dichloroacetic acid (DCA)-induced developmental toxicity and oxidative damage was examined in zebrafish embryos. Embryos were exposed to 20 mM EA administered concomitantly with 32 mM DCA at 4 hours postfertilization (hpf) and 20 h later. Embryos were observed through 144 hpf for developmental malformations, and production of superoxide anion (SA) and nitric oxide (NO) was determined in embryonic homogenates. DCA was shown to produce developmental abnormalities and significant levels of SA and NO in zebrafish embryos. EA exposure alleviated the developmental malformations observed in treated embryos and decreased the levels of SA and NO in those same embryos. Less than 10% of DCA + EA exposed embryos showed developmental malformations compared to 100% of embryos treated with DCA alone. Animals in this group that developed malformations were shown to have fewer defects than those treated with DCA only. Taken together, the results confirm the involvement of oxidative stress in the developmental toxicity of DCA in zebrafish embryos, and suggest possible protection against those effects with the use of antioxidants.     

Clinically Approved Iron Chelators Influence Zebrafish Mortality,Hatching Morphology and Cardiac Function

Iron chelation therapy using iron (III) specific chelators such as desferrioxamine (DFO, Desferal), deferasirox (Exjade or ICL-670), and deferiprone (Ferriprox or L1) are the current standard of care for the treatment of iron overload. Although each chelator is capable of promoting some degree of iron excretion, these chelators are also associated with a wide range of well documented toxicities. However, there is currently very limited data available on their effects in developing embryos. In this study, we took advantage of the rapid development and transparency of the zebrafish embryo, Danio rerio to assess and compare the toxicity of iron chelators. All three iron chelators described above were delivered to zebrafish embryos by direct soaking and their effects on mortality, hatching and developmental morphology were monitored for 96 hpf. To determine whether toxicity was specific to embryos, we examined the effects of chelator exposure via intra peritoneal injection on the cardiac function and gene expression in adult zebrafish. Chelators varied significantly in their effects on embryo mortality, hatching and morphology. While none of the embryos or adults exposed to DFO were negatively affected, ICL -treated embryos and adults differed significantly from controls, and L1 exerted toxic effects in embryos alone. ICL-670 significantly increased the mortality of embryos treated with doses of 0.25 mM or higher and also affected embryo morphology, causing curvature of larvae treated with concentrations above 0.5 mM. ICL-670 exposure (10 µL of 0.1 mM injection) also significantly increased the heart rate and cardiac output of adult zebrafish. While L1 exposure did not cause toxicity in adults, it did cause morphological defects in embryos at 0.5 mM. This study provides first evidence on iron chelator toxicity in early development and will help to guide our approach on better understanding the mechanism of iron chelator toxicity.     

Developmental toxicity of triclocarban in zebrafish (Danio rerio) embryos

Triclocarban (TCC), which is used as an antimicrobial agent in personal care products, has been widely detected in aquatic ecosystems. However, the consequence of TCC exposure on embryo development is still elusive. Here, by using zebrafish embryos, we aimed to understand the developmental defects caused by TCC exposure. After exposure to 0.3, 30, and 300 μg/L TCC from 4‐hour postfertilization (hpf) to 120 hpf, we observed that TCC exposure significantly increased the mortality and malformation, delayed hatching, and reduced body length. Exposure to TCC also affected the heart rate and expressions of cardiac development–related genes in zebrafish embryos. In addition, TCC exposure altered the expressions of the genes involved in hormonal pathways, indicating its endocrine disrupting effects. In sum, our data highlight the impact of TCC on embryo development and its interference with the hormone system of zebrafish.