Cerebral protection during fetal-to-neonatal transition under hypoxic atmosphere

Newborn asphyxia is a complication during the perinatal period. The use of O 2 for resuscitation has been broadly used in clinic. However, it has been demonstrated that oxygen overexposure induces oxidative stress (OS). We speculate that delaying postnatal in the extrauterine oxygenation status would preserve reducing equivalents, enhance redox adaptation, and protect oxyregulator tissues. The objective is evaluated OE status, induced by Fetal-Neonatal Transition (FNT) under different FiO 2 conditions, in brain. FiO 2 in pregnant mice was reduced from 21% to 14% or not the night before of delivery (G19). 8 hours after birth both group were led to room air (Hx14/21 and Nx21/21 groups) or hyperoxia (FiO 2 =100%) (Hx14/100 and Nx21/100 groups) and reset to 21% after 1 hour. The pups were sacrificed P1. We have determinated OS biomarkers (GSH/GSSG, Cysteine/ Cystine, Homocysteine/Homocystine), protein (m-tyr and o-tyr/Phe, 3NO2-tyr and 3Cl-tyr/tyr), and DNA (8OH-dG/2-dG) damage by HPLC-MS/MS and we have done a mitocondrial morphology study using ME. The results show a higher OS in the Nx21/100 group compared to the Hx14/100 group that decreases. The group Hx14/21 and Hx14/100 present a better mitochondrialcharacteristics compared to environmental conditions and their subsequent reoxygenation. Our results support that FNT under hypoxic conditions could be protective to face a possible event of newborn resuscitation.