Ethoprophos induces cardiac toxicity in zebrafish embryos

Ethoprophos is an effective and widely pesticide that used in controlling nemathelminth and soil insect. However, ethoprophos has been frequently detected in environment and freshwater. The potential toxicity to aquatic organisms is still not be explored. In this study, zebrafish embryo model was us...

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Autores principales: Meifeng Li, Tingting Yu, Jingli Lai, Xue Han, Jihuan Hu, Zeyuan Deng, Dongming Li, Zuocheng Ye, Shanghong Wang, Chengyu Hu, Xiaowen Xu
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Publicado: Elsevier 2021
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spelling oai:doaj.org-article:722bf8e046b74edcbe5240b5000e6a0d2021-11-28T04:27:28ZEthoprophos induces cardiac toxicity in zebrafish embryos0147-651310.1016/j.ecoenv.2021.113029https://doaj.org/article/722bf8e046b74edcbe5240b5000e6a0d2021-12-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S0147651321011416https://doaj.org/toc/0147-6513Ethoprophos is an effective and widely pesticide that used in controlling nemathelminth and soil insect. However, ethoprophos has been frequently detected in environment and freshwater. The potential toxicity to aquatic organisms is still not be explored. In this study, zebrafish embryo model was used to evaluated the toxicity of ethoprophos during cardiovascular developmental process of zebrafish. Zebrafish embryos were separately exposed to 10 mg/L, 20 mg/L, 30 mg/L, 40 mg/L and 50 mg/L of ethoprophos exposure at 96 h post-fertilization (hpf), which induced cardiac defects, such as low heart rate, pericardium edema and long SV-BA distance, but had no influence to vascular development. Mechanistically, the expression of cardiac-related genes were abnormal. Moreover, ethoprophos exposure significantly increased oxidative stress in zebrafish embryos by inhibiting the production of antioxidant enzyme (SOD) and activating reactive oxygen species. Expectedly, some apoptosis genes were induced and the apoptotic cardiomyocytes were detected by acridine orange staining. In addition, ethoprophos exposure also inhibited the expression of genes in wnt signaling pathway, such as β-catenin, Axin2, GSK3β and Sox9b. BML284, an activator of wnt signaling pathway, can rescue the cardiotoxic effect of embryos. These results indicated that oxidative stress and blocking wnt signaling pathway were molecular basis of ethoprophos-induced injure in zebrafish. Generally, our study showed that ethoprophos exposure led to severe cardiotoxicity to zebrafish embryo.Meifeng LiTingting YuJingli LaiXue HanJihuan HuZeyuan DengDongming LiZuocheng YeShanghong WangChengyu HuXiaowen XuElsevierarticleEthoprophosZebrafish embryoCardiotoxicityOxidative stressWnt signaling pathwayEnvironmental pollutionTD172-193.5Environmental sciencesGE1-350ENEcotoxicology and Environmental Safety, Vol 228, Iss , Pp 113029- (2021)
institution DOAJ
collection DOAJ
language EN
topic Ethoprophos
Zebrafish embryo
Cardiotoxicity
Oxidative stress
Wnt signaling pathway
Environmental pollution
TD172-193.5
Environmental sciences
GE1-350
spellingShingle Ethoprophos
Zebrafish embryo
Cardiotoxicity
Oxidative stress
Wnt signaling pathway
Environmental pollution
TD172-193.5
Environmental sciences
GE1-350
Meifeng Li
Tingting Yu
Jingli Lai
Xue Han
Jihuan Hu
Zeyuan Deng
Dongming Li
Zuocheng Ye
Shanghong Wang
Chengyu Hu
Xiaowen Xu
Ethoprophos induces cardiac toxicity in zebrafish embryos
description Ethoprophos is an effective and widely pesticide that used in controlling nemathelminth and soil insect. However, ethoprophos has been frequently detected in environment and freshwater. The potential toxicity to aquatic organisms is still not be explored. In this study, zebrafish embryo model was used to evaluated the toxicity of ethoprophos during cardiovascular developmental process of zebrafish. Zebrafish embryos were separately exposed to 10 mg/L, 20 mg/L, 30 mg/L, 40 mg/L and 50 mg/L of ethoprophos exposure at 96 h post-fertilization (hpf), which induced cardiac defects, such as low heart rate, pericardium edema and long SV-BA distance, but had no influence to vascular development. Mechanistically, the expression of cardiac-related genes were abnormal. Moreover, ethoprophos exposure significantly increased oxidative stress in zebrafish embryos by inhibiting the production of antioxidant enzyme (SOD) and activating reactive oxygen species. Expectedly, some apoptosis genes were induced and the apoptotic cardiomyocytes were detected by acridine orange staining. In addition, ethoprophos exposure also inhibited the expression of genes in wnt signaling pathway, such as β-catenin, Axin2, GSK3β and Sox9b. BML284, an activator of wnt signaling pathway, can rescue the cardiotoxic effect of embryos. These results indicated that oxidative stress and blocking wnt signaling pathway were molecular basis of ethoprophos-induced injure in zebrafish. Generally, our study showed that ethoprophos exposure led to severe cardiotoxicity to zebrafish embryo.
format article
author Meifeng Li
Tingting Yu
Jingli Lai
Xue Han
Jihuan Hu
Zeyuan Deng
Dongming Li
Zuocheng Ye
Shanghong Wang
Chengyu Hu
Xiaowen Xu
author_facet Meifeng Li
Tingting Yu
Jingli Lai
Xue Han
Jihuan Hu
Zeyuan Deng
Dongming Li
Zuocheng Ye
Shanghong Wang
Chengyu Hu
Xiaowen Xu
author_sort Meifeng Li
title Ethoprophos induces cardiac toxicity in zebrafish embryos
title_short Ethoprophos induces cardiac toxicity in zebrafish embryos
title_full Ethoprophos induces cardiac toxicity in zebrafish embryos
title_fullStr Ethoprophos induces cardiac toxicity in zebrafish embryos
title_full_unstemmed Ethoprophos induces cardiac toxicity in zebrafish embryos
title_sort ethoprophos induces cardiac toxicity in zebrafish embryos
publisher Elsevier
publishDate 2021
url https://doaj.org/article/722bf8e046b74edcbe5240b5000e6a0d
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AT tingtingyu ethoprophosinducescardiactoxicityinzebrafishembryos
AT jinglilai ethoprophosinducescardiactoxicityinzebrafishembryos
AT xuehan ethoprophosinducescardiactoxicityinzebrafishembryos
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