1-萘酚胚胎期暴露对斑马鱼发育的毒性作用

任平平; 舒莉萍; 王一慧; 莫晶; 周艳华; 何志旭

doi:10.16016/j.1000-5404.201901133

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1-萘酚胚胎期暴露对斑马鱼发育的毒性作用

基础医学 | 更新时间：2026-01-09

- 1-萘酚胚胎期暴露对斑马鱼发育的毒性作用
- Developmental toxicity of embryonic 1-naphthol exposure in zebrafish
- 第三军医大学学报 2019年41卷第14期页码：1321-1327
- 作者机构：
  
  1.550004 贵阳，贵州医科大学:儿科学教研室
  2.550004 贵阳，贵州医科大学:组织工程与干细胞中心，中国医学科学院成体干细胞转化研究重点实验室
  3.563006 贵州遵义，遵义医科大学儿科学教研室
- 作者简介：
  
  [何志旭，E-mail:hzx@gmc.edu.cnHE Zhixu, E-mail:hzx@gmc.edu.cn
- 基金信息：
  
  国家自然科学基金面上项目(81871313);贵州省重大基础研究项目(黔科合J重大字〔2015〕2003);贵州省重大专项资金(黔科合重大专项字〔2014〕6008)
- DOI：10.16016/j.1000-5404.201901133
  中图分类号： R321-33; R994.6; R996
- 收稿：2019-01-16，
  
  修回：2019-03-12，
  
  纸质出版：2019-07-30
- 稿件说明：
移动端阅览
任平平, 舒莉萍, 王一慧, 等. 1-萘酚胚胎期暴露对斑马鱼发育的毒性作用[J]. 第三军医大学学报, 2019,41(14):1321-1327.

Pingping REN, Liping SHU, Yihui WANG, et al. Developmental toxicity of embryonic 1-naphthol exposure in zebrafish[J]. Journal of Third Military Medical University, 2019, 41(14): 1321-1327.
任平平, 舒莉萍, 王一慧, 等. 1-萘酚胚胎期暴露对斑马鱼发育的毒性作用[J]. 第三军医大学学报, 2019,41(14):1321-1327. DOI： 10.16016/j.1000-5404.201901133.

Pingping REN, Liping SHU, Yihui WANG, et al. Developmental toxicity of embryonic 1-naphthol exposure in zebrafish[J]. Journal of Third Military Medical University, 2019, 41(14): 1321-1327. DOI： 10.16016/j.1000-5404.201901133.

摘要

目的

探讨1-萘酚(1-NAP)胚胎期暴露对斑马鱼发育的毒性作用，并对其可能的机制进行研究。

方法

挑选斑马鱼受精卵，在受精后24 h(hours post fertilization

hpf)进行不同浓度(0、40、80、160、200 μmol/L)1-NAP暴露处理，观察并记录其处理至斑马鱼120 hpf时的畸形数和死亡数，计算畸形率、孵化率及半数致死浓度(IC

)。设置空白对照组，N-乙酰半胱氨酸(NAC)处理组，1-NAP处理组，NAC预处理组，检测幼鱼体内活性氧(ROS)、丙二醛(MDA)、还原型谷胱甘肽(GSH)和总巯基(-SH)含量以及超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性；通过Western blot法检测胚胎凋亡蛋白Caspase3、Bax的表达情况。

结果

计算出1-NAP在斑马鱼胚胎的IC

为111.31 μmol/L，斑马鱼胚胎期暴露于高浓度1-萘酚(＞80 μmol/L)导致死亡率和畸形率明显增加，孵化率明显降低，表现出发育毒性；50 μmol/L浓度1-NAP处理组ROS、MDA含量明显升高，GSH、-SH水平明显降低，抗氧化酶CAT、SOD的活性受到抑制(

＜0.001)；胚胎凋亡蛋白Caspase3、Bax表达量增加；NAC(0.5 mmol/L)预处理组斑马鱼胚胎的畸形率明显降低，ROS、MDA含量明显减少，GSH、-SH含量以及SOD、CAT活性有所恢复，凋亡蛋白Caspase3、Bax表达量明显降低。

结论

1-萘酚胚胎期暴露对斑马鱼发育的毒性作用可能与1-萘酚诱导的氧化应激相关。

Abstract

Objective

To investigate the toxic effects of embryonic exposure to 1-naphthol (1-NAP) on zebrafish development and explore the possible mechanism.

Methods

Fertilized zebrafish eggs were exposed to 1-NAP at the concentrations of 40

160 and 200 μmol/L on 24 h post fertilization (hpf). The numbers of zebrafish malformations and deaths were recorded at 120 hpf

and the deformity rate

hatching rate and the median lethal concentration (IC

) of 1-NAP were calculated. The hatched zebrafish with or without embryonic exposure to 50 μmol/L 1-NAP and pretreatment with N-acetylcysteine (NAC) were examined for levels of reactive oxygen species (ROS)

malondialdehyde (MDA)

reduced glutathione (GSH)

total sulfhydryl

and activities of superoxide dismutase (SOD) and catalase (CAT); Western blotting was performed to detect the expression of Caspase-3 and Bax.

Results

The IC

of 1-NAP in zebrafish embryos was 111.31 μmol/L

and the zebrafish embryos exposed to high-concentration (

80 μmol/L) 1-NAP exhibited obviously increased mortality and deformity rates with a significantly reduced hatch

ing rate

demonstrating significant developmental toxicity of 1-NAP. Embryonic exposure to 50 μmol/L 1-NAP significantly increased the levels of ROS and MDA

lowered the levels of GSH and total sulfhydryl

suppressed the activities of antioxidant enzymes CAT and SOD (

0.001)

and decreased the expression levels of Caspase-3 and Bax in the hatched zebrafish. The zebrafish embryos pretreated with 0.5 mmol/L NAC prior to 1-NAP exposure showed a significantly decreased abnormality rate with obviously lowered ROS and MDA levels

restoration of GSH and total sulfhydryl content and SOD and CAT activities

and obviously reduced expression levels of Caspase-3 and Bax.

Conclusion

The developmental toxicity of 1-NAP in zebrafish embryos is probably associated with enhanced oxidative stress induced by 1-NAP.

关键词

Keywords

references

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