Toxic effects of polychlorinated biphenyls on cardiac development in zebrafish

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• 作者：Mengmeng Li (1)
  Xuejie Wang (1)
  Jingai Zhu (1)
  Shasha Zhu (1)
  Xiaoshan Hu (1)
  Chun Zhu (1)
  Xirong Guo (1)
  Zhangbin Yu (1)
  Shuping Han (1)
  
  1. State Key Laboratory of Reproductive Medicine ; Department of Pediatrics ; Nanjing Maternity and Child Health Care Hospital Affiliated to Nanjing Medical University ; Nanjing ; 210029 ; China
  
• 关键词：Zebrafish ; Polychlorinated biphenyls ; Heart ; Development ; Signaling pathway
• 刊名：Molecular Biology Reports
• 出版年：2014
• 出版时间：December 2014
• 年：2014
• 卷：41
• 期：12
• 页码：7973-7983
• 全文大小：1,020 KB
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• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Life Sciences
  Animal Anatomy, Morphology and Histology
  Animal Biochemistry
  
• 出版者：Springer Netherlands
• ISSN：1573-4978

文摘

Polychlorinated biphenyls (PCBs) are ubiquitous environmental pollutants that may pose significant health-risks to various organisms including humans. Although the mixed PCB Aroclor 1254 is widespread in the environment, its potential toxic effect on heart development and the mechanism underlying its developmental toxicity have not been previously studied. Here, we used the zebrafish as a toxicogenomic model to examine the effects of Aroclor 1254 on heart development. We found that PCB exposure during zebrafish development induced heart abnormalities including pericardial edema and cardiac looping defects. Further malformations of the zebrafish embryo were observed and death of the larvae occurred in a time- and dose-dependent manner. Our mechanistic studies revealed that abnormalities in the arylhydrocarbon receptor, Wnt and retinoic acid signaling pathways may underlie the effects of PCBs on zebrafish heart development. Interestingly, co-administration of Aroclor 1254 and diethylaminobenzaldehyde, an inhibitor of retinaldehyde dehydrogenase, partially rescued the toxic effects of PCBs on zebrafish heart development. In conclusion, PCBs can induce developmental defects in the zebrafish heart, which may be mediated by abnormal RA signaling.