The effect of tris (1,3-dichloro-2-propyl) phosphate on the early embryonic heart development of Oryzias melastigma

被引：0
作者：
Wang, Sujing [1 ]
Zheng, Na [1 ]
An, Qirui [1 ]
Li, Xiaoqian [1 ]
Ji, Yining [1 ]
Li, Yunyang [2 ]
Chen, Changcheng [1 ]
Xiu, Zhifei [1 ]
机构：
[1] Key Laboratory of Groundwater Resources and Environment of the Ministry of Education, College of Environment and Resources, Jilin University
[2] Northeast Institute of Geography and Agricultural Ecology, Chinese Academy of Sciences, Jilin, Changchun
来源：
Science of the Total Environment | 2024年 / 955卷
基金：
中国国家自然科学基金;
关键词：
Cardiotoxicity; Marine medaka; Oxidative stress; TDCIPP; Vitellogenin;
D O I：
10.1016/j.scitotenv.2024.177313
中图分类号：
学科分类号：
摘要：
The flame retardant tri (1, 3-dichloro-2-propyl) phosphate (TDCIPP) is widely present in environmental media and organisms. People have paid much attention to the growth and developmental toxicity of TDCIPP, but there is little information about its cardiotoxicity and potential mechanisms. In this study, marine medaka (Oryzias melastigma) embryos were exposed to TDCIPP solutions (0, 0.05, 0.5, 5, and 50 μg/L) for 21 days to investigate the adverse effects of TDCIPP on cardiac development. The results showed that TDCIPP exposure altered the heart rate at different stages of embryonic development. In addition, 50 μg/L TDCIPP resulted in increased sinus venosus (SV)–bulbus arteriosus (BA) distance, pericardial cysts, and cardiac linearization in newly hatched fish. During embryonic development, the expression level of key genes regulating cardiac development is disturbed. The early stage of cardiac development is the sensitive window period for the toxic effects of TDCIPP. Oxidative stress was observed in newly hatched juveniles, but no significant lipid peroxidation damage was observed. In addition, vitellogenin (VTG) levels in juvenile fish were significantly reduced. Our results show that TDCIPP exposure induces cardiotoxicity in marine medaka embryos, which is induced in the early stages and promotes heart defects by amplifying inflammatory responses at a later stage. © 2024
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