Alcohol exposure during pregnancy induces cardiac mitochondrial damage in offspring mice

作者全名：Su, Yujuan; Yu, Yujuan; Quan, Junjun; Zhang, Junjie; Xu, Ying

作者地址：[Su, Yujuan; Yu, Yujuan; Quan, Junjun; Zhang, Junjie; Xu, Ying] Chongqing Med Univ, Childrens Hosp, Minist Educ, Chongqing Key Lab Pediat,Dept Resp Med,Natl Clin R, 136 Zhongshan Er Rold, Chongqing 400014, Peoples R China

通信作者：Xu, Y (通讯作者)，Chongqing Med Univ, Childrens Hosp, Minist Educ, Chongqing Key Lab Pediat,Dept Resp Med,Natl Clin R, 136 Zhongshan Er Rold, Chongqing 400014, Peoples R China.

来源：BIRTH DEFECTS RESEARCH

ESI学科分类：MOLECULAR BIOLOGY & GENETICS

WOS号：WOS:001246421200001

JCR分区：Q4

影响因子：1.6

年份：2024

卷号：116

期号：6

开始页：　

结束页：　

文献类型：Article

关键词：alcohol; cardiac damage; mitochondrial dysfunction; prenatal ethanol exposure

摘要：BackgroundPrenatal alcohol exposure (PAE) has been linked to congenital heart disease and fetal alcohol syndrome. The heart primarily relies on mitochondria to generate energy, so impaired mitochondrial function due to alcohol exposure can significantly affect cardiac development and function. Our study aimed to investigate the impact of PAE on myocardial and mitochondrial functions in offspring mice.MethodsWe administered 30% alcohol (3 g/kg) to pregnant C57BL/6 mice during the second trimester. We assessed cardiac function by transthoracic echocardiography, observed myocardial structure and fibrosis through staining tests and electron transmission microscopy, and detected cardiomyocyte apoptosis with dUTP nick end labeling assay and real-time quantitative PCR. Additionally, we measured the reactive oxygen species content, ATP level, and mitochondrial DNA copy number in myocardial mitochondria. Mitochondrial damage was evaluated by assessing the level of mitochondrial membrane potential and the opening degree of mitochondrial permeability transition pores.ResultsOur findings revealed that PAE caused cardiac systolic dysfunction, ventricular enlargement, thinned ventricular wall, cardiac fibrosis in the myocardium, scattered loss of cardiomyocytes, and disordered arrangement of myocardial myotomes in the offspring. Furthermore, we observed a significant increase in mitochondrial reactive oxygen species content, a decrease in mitochondrial membrane potential, ATP level, and mitochondrial DNA copy number, and sustained opening of mitochondrial permeability transition pores in the heart tissues of the offspring.ConclusionsThese results indicated that PAE had adverse effects on the cardiac structure and function of the newborn mice and could trigger oxidative stress in their myocardia and contribute to mitochondrial dysfunction.

基金机构：Chongqing Science and Technology Bureau, Chongqing Municipal Health Commission; Chongqing Municipal Science and Technology Commission [CSTB2022TIAD-GPX0007]; [2023DBXM003]

基金资助正文：This project was supported by the Chongqing Science and Technology Bureau, Chongqing Municipal Health Commission (No. 2023DBXM003) and the Chongqing Municipal Science and Technology Commission (No. CSTB2022TIAD-GPX0007).