Di-(2-ethylhexyl) Phthalate Exposure Induces Developmental Toxicity in the Mouse Fetal Heart via Mitochondrial Dysfunction.

IF 3.4 3区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Cardiovascular Toxicology Pub Date : 2024-10-25 DOI:10.1007/s12012-024-09936-4
Yafei Guo, Bowen Li, Yu Yan, Nanjun Zhang, Shuran Shao, Lixia Yang, Lixue Ouyang, Ping Wu, Fan Ma, Hongyu Duan, Kaiyu Zhou, Yimin Hua, Chuan Wang
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Abstract

Congenital heart disease (CHD) is a major cause of infant mortality and morbidity, with growing interest in the role of environmental factors in its etiology. Di-(2-ethylhexyl) phthalate (DEHP), an environmental endocrine disruptor, has been implicated in the development of CHD. This study aimed to investigate the effects of DEHP exposure on fetal heart development in mice. Pregnant mice exposed to DEHP exhibited increased fetal malformations, decreased fetal weight, and reduced crown-rump length.f Transcriptomic analysis revealed the downregulation of genes involved in aerobic respiration and mitochondrial ATP synthesis. Functional assays demonstrated reduced mitochondrial respiration, decreased ATP production, elevated reactive oxygen species levels, and lowered mitochondrial membrane potential in DEHP-exposed fetal cardiomyocytes. These findings underscore the detrimental effects of DEHP on fetal cardiac health and provide insights into the molecular mechanisms underlying DEHP-induced CHD. Understanding these mechanisms is crucial for developing preventive strategies against environmental toxicants that affect fetal cardiac development.

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邻苯二甲酸二(2-乙基己酯)暴露通过线粒体功能障碍诱发小鼠胎儿心脏的发育毒性
先天性心脏病(CHD)是婴儿死亡和发病的主要原因之一,人们越来越关注环境因素在其病因中的作用。邻苯二甲酸二(2-乙基己基)酯(DEHP)是一种环境内分泌干扰物,被认为与先天性心脏病的发病有关。本研究旨在调查接触 DEHP 对小鼠胎儿心脏发育的影响。转录组分析显示,参与有氧呼吸和线粒体 ATP 合成的基因下调。功能测试显示,在暴露于 DEHP 的胎儿心肌细胞中,线粒体呼吸减少,ATP 生成减少,活性氧水平升高,线粒体膜电位降低。这些发现强调了DEHP对胎儿心脏健康的有害影响,并提供了对DEHP诱发先天性心脏病的分子机制的见解。了解这些机制对于制定针对影响胎儿心脏发育的环境毒物的预防策略至关重要。
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来源期刊
Cardiovascular Toxicology
Cardiovascular Toxicology 医学-毒理学
CiteScore
6.60
自引率
3.10%
发文量
61
审稿时长
>12 weeks
期刊介绍: Cardiovascular Toxicology is the only journal dedicated to publishing contemporary issues, timely reviews, and experimental and clinical data on toxicological aspects of cardiovascular disease. CT publishes papers that will elucidate the effects, molecular mechanisms, and signaling pathways of environmental toxicants on the cardiovascular system. Also covered are the detrimental effects of new cardiovascular drugs, and cardiovascular effects of non-cardiovascular drugs, anti-cancer chemotherapy, and gene therapy. In addition, Cardiovascular Toxicology reports safety and toxicological data on new cardiovascular and non-cardiovascular drugs.
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