Use of maternal
oxygen for intrauterine
resuscitation is contentious because of the lack of evidence for its efficacy and the possibility of fetal harm through oxidative stress. Because the developing brain is rich in
lipids and low in
antioxidants, it remains vulnerable to oxidative stress. Here, we tested this hypothesis in a term pregnant rat model with
oxytocin-induced
fetal distress followed by treatment with either room air or 100%
oxygen for 6 h. Fetal brains from both sexes were subjected to assays for
biomarkers of oxidative stress (4-hydroxynonenal, protein carbonyl, or 8-hydroxy-2'-deoxyguanosine), expression of genes mediating oxidative stress, and mitochondrial oxidative phosphorylation. Contrary to our hypothesis, maternal
hyperoxia was not associated with increased
biomarkers of oxidative stress in the fetal brain. However, there was significant upregulation of the expression of select genes mediating oxidative stress, of which some were male-specific. These observations, however, were not accompanied by changes in the expression of
proteins from the mitochondrial electron transport chain. In summary, maternal
hyperoxia in the setting of acute uteroplacental
ischemia-
hypoxia does not appear to cause oxidative damage to the developing brain.