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

文献类型： 外文期刊

第一作者： Hong, Xiangsheng

作者： Hong, Xiangsheng;Li, Jiasu;Zha, Jinmiao;Yuan, Lilai;Zhao, Xu;Shan, Yuan;Shan, Yuan;Qin, Tianlong;Zha, Jinmiao

作者机构：

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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