Related Experiment Video
Updated: Jul 27, 2026
Construction of Vapor Chambers Used to Expose Mice to Alcohol During the Equivalent of all Three Trimesters of Human Development
Published on: July 13, 2014
Alcohol exposure during pregnancy induces cardiac mitochondrial damage in offspring mice
Yujuan Su1, Yujuan Yu1, Junjun Quan1
1Department of Anesthesiology, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatrics, Children's Hospital of Chongqing Medical University, Chongqing, China.
Insights
Prenatal alcohol exposure (PAE) harms offspring heart development, causing cardiac dysfunction and mitochondrial damage. This study in mice reveals PAE-induced oxidative stress and impaired energy production in the heart.
Area of Science:
- Cardiovascular Biology
- Mitochondrial Medicine
- Developmental Toxicology
Background:
- Prenatal alcohol exposure (PAE) is associated with congenital heart defects and fetal alcohol syndrome.
- Mitochondrial dysfunction is a key factor in alcohol's impact on cardiac development and function.
Purpose of the Study:
- To investigate the effects of PAE on myocardial and mitochondrial functions in offspring mice.
Main Methods:
- Administered alcohol to pregnant mice during the second trimester.
- Assessed cardiac function, myocardial structure, fibrosis, and apoptosis in offspring.
- Measured mitochondrial oxidative stress, ATP levels, DNA copy number, membrane potential, and pore opening.
Main Results:
- PAE led to cardiac systolic dysfunction, ventricular enlargement, fibrosis, and cardiomyocyte loss.
- Observed increased mitochondrial reactive oxygen species and sustained opening of permeability transition pores.
- Detected decreased mitochondrial membrane potential, ATP levels, and mitochondrial DNA copy number.
Conclusions:
- PAE adversely affects neonatal mouse cardiac structure and function.
- PAE induces myocardial oxidative stress and mitochondrial dysfunction in offspring.
Background:
Prenatal 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.
Methods:
We 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.
Results:
Our 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.
Conclusions:
These 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.
