Dimethyl phthalate induced cardiovascular developmental toxicity in zebrafish embryos by regulating MAPK and calcium signaling pathways

• Published in: The Science of the total environment 2024-05, Vol.926, p.171902-171902, Article 171902
• Main Authors: Cao, Bianneng, Kong, Haotian, Shen, Chuanlin, She, Gaimei, Tian, Shuimiao, Liu, Haojie, Cui, Lishuang, Zhang, Yun, He, Qiuxia, Xia, Qing, Liu, Kechun
• Format: Article
• Language: English
• Subjects: Cardiovascular developmental toxicity; Dimethyl phthalate; Transcriptome sequencing; Zebrafish
• ISSN: 0048-9697; 1879-1026
• DOI: 10.1016/j.scitotenv.2024.171902

Dimethyl phthalate (DMP), the lowest-molecular-weight phthalate ester (PAE), is one of the most commonly detected persistent organic pollutants in the environment, but its toxic effects, especially cardiovascular developmental toxicity, are largely unknown. In this study, zebrafish embryos were exposed to sublethal concentrations of DMP from 4 to 96 hpf. Our results showed that DMP treatment induced yolk retention, pericardial edema, and swim bladder deficiency, as well as increased SV-BA distance and decreased heart rate, stroke volume, ventricular axis shortening rate and ejection fraction. In addition, oxidative stress and apoptosis were found to be highly involved in this process. The results of transcriptome sequencing and mRNA expression of related genes indicated that MAPK and calcium signaling pathways were perturbed by DMP. These findings have the potential to provide new insights into the potential developmental toxicity and cardiovascular disease risk of DMP. [Display omitted] •DMP induced developmental toxicity at sublethal concentrations in zebrafish.•DMP triggered severe cardiovascular developmental defects in zebrafish embryos.•Cell apoptosis and oxidative stress damage were observed under DMP exposure.•MAPK and calcium signaling pathways were dysregulated after DMP exposure.