Transient uterine hypercontractility causes oxidative stress in the fetal brain, sex-dependent mitochondrial abnormalities, and altered social behavior of adolescent male rat offspring

The neurodevelopmental impact of transient ischemic-hypoxemic insults is poorly understood. Here, we simulated placental ischemia-hypoxemia via oxytocin-induced uterine hypercontractility to show a profound decrease in placental perfusion/oxygenation, oxidative stress in the fetal brain, sex-dependent differences in gene expression mediating oxidative stress, and persistent upregulation of mitochondrial oxidative phosphorylation proteins in the anterior cingulate cortex along with social behavioral impairment especially in male offspring.