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Embryonic Exposure to Organophosphate Flame Retardants (OPFRs) Differentially Induces Cardiotoxicity in Rare Minnow (Gobiocypris rarus)

文献类型： 外文期刊

作者： Hong, Xiangsheng 1 ; Yuan, Lilai 2 ; Zhao, Xu 3 ; Shan, Yuan 4 ; Qin, Tianlong 6 ; Li, Jiasu 1 ; Zha, Jinmiao 1 ;

作者机构： 1.Chinese Acad Sci, Natl Engn Res Ctr Ind Wastewater Detoxicat & Resou, Res Ctr Ecoenvironm Sci, Beijing 100085, Peoples R China

2.Chinese Acad Fishery Sci, Fishery Resource & Environm Res Ctr, Beijing 100141, Peoples R China

3.Minist Environm Protect Peoples Republ China, South China Inst Environm Sci, State Environm Protect Key Lab Environm Pollut Hlt, Guangzhou 510655, Peoples R China

4.Natl Fisheries Technol Extens Ctr, Beijing 100125, Peoples R China

5.China Soc Fisheries, Beijing 100125, Peoples R China

6.Aquat Technol Promot Guidance Ctr Wuhan, Wuhan 430014, Peoples R China

7.Univ Chinese Acad Sci, Beijing 100049, Peoples R China

关键词： flame retardants; embryotoxicity; bradycardia; mAChR; Ca2+ channels; Na+ channels; molecular mechanism

期刊名称：ENVIRONMENTAL SCIENCE & TECHNOLOGY （ 影响因子：10.8； 五年影响因子：11.6 ）

ISSN： 0013-936X

年卷期： 2024 年 58 卷 31 期

页码：

收录情况： SCI

摘要： Organophosphorus flame retardants (OPFRs) such as triphenyl phosphate (TPHP) and tris(1,3-dichloro-2-propyl) phosphate (TDCIPP) were reported to impair cardiac function in fish. However, limited information is available regarding their cardiotoxic mechanisms. Using rare minnow (Gobiocypris rarus) as a model, we found that both TPHP and TDCIPP exposures decreased heart rate at 96 h postfertilization (hpf) in embryos. Atropine (an mAChR antagonist) can significantly attenuate the bradycardia caused by TPHP, but only marginally attenuated in TDCIPP treatment, suggesting that TDCIPP-induced bradycardia is independent of mAChR. Unlike TDCIPP, although TPHP-induced bradycardia could be reversed by transferring larvae to a clean medium, the inhibitory effect of AChE activity persisted compared to 96 hpf, indicating the existence of other bradycardia regulatory mechanisms. Transcriptome profiling revealed cardiotoxicity-related pathways in treatments at 24 and 72 hpf in embryos/larvae. Similar transcriptional alterations were also confirmed in the hearts of adult fish. Further studies verified that TPHP and TDCIPP can interfere with Na+/Ca2+ transport and lead to disorders of cardiac excitation-contraction coupling in larvae. Our findings provide useful clues for unveiling the differential cardiotoxic mechanisms of OPFRs and identifying abnormal Na+/Ca2+ transport as one of a select few known factors sufficient to impair fish cardiac function.

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