Transient uterine hypercontractility causes oxidative stress in the fetal brain and sex-dependent mitochondrial and behavioral abnormalities in adolescent male rat offspring

The neurodevelopmental impact of transient ischemic-hypoxemic insult during labor is poorly understood. Here, using an oxytocin-induced uterine hypercontractility paradigm, we confirm transient uteroplacental compromise, increased oxidative stress in the fetal brain, and enduring social behavioral impairment in male offspring with persistent upregulation of mitochondrial proteins in the anterior cingulate cortex. Our findings, therefore, indicate persistent mitochondrial dysfunction as a possible mechanistic link between intrauterine asphyxia and neurodevelopmental disorders.